4^th Global Summit on Toxicology August 24-26, 2015 Philadelphia, USA

Biography:

Shailesh P Banerjee received his PhD in Pharmacology from University of Toronto and a MPH degree from the Columbia University. He has served as an Associate Editor of the Journal of Neuroscience 1981-84. He has been in in the Medical School Faculty in either University of Rochester School of Medicine or CUNY Medical School for last forty years or more and published more than 100 scientific research papers in reputed journals.

Abstract:

Taurine is an inhibitory neuromodulatory endogenous amino-acid in the CNS and activates GABA- and glycine-insensitive chloride channel and inhibits the glutamate NMDA receptor. We investigated taurine’s interaction with the NMDA receptor using electrophysiological, receptor binding studies and explored its long-term effects by using western blot determination of NMDA and AMPA receptor subunits expression in the rat frontal cortex. Taurine was found to modulate NMDA receptor function without affecting AMPA receptor mediated activity perhaps by partially blocking spermine-potentiated NMDA receptor activation. Furthermore, our studies revealed that inhibition of evoked responses by taurine overlapped with that by Ro-25-6981, a selective antagonist for the GLuN1/GLuN2B NMDA receptor subtype, suggesting that taurine modulates NMDA receptor by acting on the NMDA GLuN1/GLuN2B receptor subunit (s). This observation was confirmed by conducting receptor binding studies using tritiated- spermidine or-taurine that showed that taurine and polyamines may interact at a common binding site. Chronic administration of taurine caused significantincrease in the expression of NMDA GLuN2B, but not GLuN1 subunit and a significant decrease in the expression of the AMPA GLuR2 subunit. The up-regulation of the GLuN2B subunit suggests a consequence of its possible long-term interaction with taurine, and the down-regulation of the AMPA GLuR2 subunit is possibly correlated to an increased recruitment of the GLuR2-subunit-lacking, calcium-permeable subtype of AMPA receptor. Other studies in our laboratory showed that taurine is an effective anti-cataleptic and neuro-protective agent. Also, micro dialysis investigation of effects chronic administration of psychotropic drug, cocaine revealed an increase in extracellular release of endogenous taurine which may protect against deleterious effects of the substances of abuse. In addition, taurine administration was found to prevent cocaine-induced addiction by suppressing spontaneous locomotor activity and conditioned place preference. Thus taurine is a unique psychopharmacological compound with potential for a variety of therapeutic uses including as a neuro-protective, anti-cataleptic, and anti-addicting agent.

Biography:

Marketa Bebarova has completed her MD studies at the age of 25 years and her PhD studies at the age of 29 years, both at Masaryk University (Czech Republic). Subsequently, she passed a Postdoctoral research stay at Cardiovascular Research Institute Maastricht, Maastricht University (Netherlands). Nowadays, she serves as an Associate Professor and as the Head of Laboratory of Cellular Electrophysiology at Department of Physiology, Faculty of Medicine, Masaryk University. She has published 20 papers in reputed journals. She is a nucleus member of the European Working Group (WG) on Cardiac Cellular Electrophysiology (WG of the European Society of Cardiology).

Abstract:

Alcohol intoxication may induce electrocardiographic changes and arrhythmias, most frequently the atrial fibrillation (AF). In the pathogenesis of arrhythmias including AF, modifications and/or heterogeneity of inward rectifier potassium currents, namely IK1 and acetylcholine-sensitive current IK(Ach), are known to be involved. Recently, we have reported that ethanol at clinically relevant concentrations alters the rat ventricular IK1 in a dual way. We have also observed a significant inhibitory effect of acetaldehyde, the primary metabolite of ethanol, on this current. Considering missing data, we aimed to analyze ethanol-induced changes of inward rectifiers in the cardiac atria. Experiments were performed by the whole-cell patch clamp technique at room temperature in enzymatically isolated rat atrial myocytes. In contrast to the ventricular IK1, ethanol in concentrations of 20 and 80 mM (0.09 and 0.4%) showed only minor average changes of the atrial IK1. In the case of IK(Ach), both components of this current, i.e. the constitutively active and the acetylcholine-induced IK(Ach), were affected by ethanol. The constitutively active IK(Ach) was significantly increased at all examined concentrations between 2 and 80 mM (e.g. at 20 mM by 114.6±28.3%). The acetylcholine-induced IK(Ach) was affected by 8 to 80 mM ethanol in a dual way with its prevailing activation (e.g. by 29.2±17.3% at 20 mM). To conclude, the effect of ethanol on the atrial IK1 was minor compared to its effect on the ventricular IK1. Changes of the atrial electrophysiology under alcohol intoxication are likely caused by other factors, the clinically relevant action of ethanol on IK(Ach) may contribute.

Biography:

Peizhen Janet Song received her PhD from the University of Kansas, School of Medicine and her Medical Doctor degree from Shanxi Medical University. As a principal in QNS consulting, LLT, She has contributed to the success of numerous projects for her clients which include some global giants in the pharmaceutical world. Her expertise lies in R&D and regulatory affairs in life science related fields.

Abstract:

Recently, the discovery of bile acid sequestrant (BAS) as a novel anti-diabetes medication places renewed emphasis on the need for more research on the mechanism by which BASs play their pharmacological roles. BASs are non-absorbable resins and function by contraction of the bile acid (BA) pool in the body. Herein, we hypothesize that BASs exert their pharmacological function by altering serum BA composition and BA signaling in the body. Mice were fed 2% Cholestyramine (resin) in their diets for one week. The individual BA concentration and mRNAs of genes involved in BA signaling were quantified. As expected, the resin reduced total BA concentration in the liver 80%. But surprisingly, the resin increased the concentrations of CA and T-CA in the serum, causing a slightly increased total BA concentration in the serum. The mRNA of the BA-biosynthesis enzymes, Cyp7a1 and Cyp8b1, increased 180 and 100% respectively after resin feeding. However, the FXR-target gene SHP in the liver was not decreased. In contrast, the ileum Fgf15 mRNA expression was significantly decreased. Feeding the resin did not alter the BA uptake transporters on the sinusoidal membrane nor did it altered the efflux transporters on the canalicular membrane, whereas, the efflux transporters on the sinusoidal membrane of hepatocytes, Mrp 3 and 4, were increased by the resin 22 and 150% respectively. In ileum, feeding the resin increased the uptake transporter, Asbt, 66%. Collectively, the data suggest that increased expression of Cyp7a1 and Cyp8b1 in mouse liver by resin administered through the diet appears to be due to a decrease in the ileum Fgf15 signaling, rather than a decrease in hepatic FXR signaling. In addition, the increased concentration of CA in the serum may play a role in the hypoglycemic effects of the resin.

Biography:

Balszuweit F is a pharmacist and obtained his PhD at the Free University Berlin in 2005. Along with his research activities within the Bundeswehr Medical Service, he has been concerned with research management, regulatory affairs and scientific cooperation. His research interests are focused on cell co-cultures to identify novel treatment strategies, in particular against sulfur mustard injuries.

Abstract:

Sulfur mustard (SM) is a vesicating chemical warfare agent causing skin blistering, ulceration, impaired wound healing, prolonged hospitalization and permanent lesions. Silibinin, the lead compound from Silybum marianum, has been discussed as a potential antidote to SM poisoning, but previous investigations had been limited to nitrogen mustards. Water solubility of silibinin is poor, thus a water-soluble prodrug, e.g. silibinin-bis-succinat (silibinin-BS, SIL-BS) should be desirable for rapid bioavailability as an antidote. HaCaT cells were exposed to SM (30, 100, and 300 μM) for 30min and treated thereafter with SIL-BS (10, 50, and 100μM) for 24h. Necrosis, apoptosis and production interleukin-6 and -8 were determined. SIL-BS dose-dependently reduced SM cytotoxicity, even after 300 μM exposure. Doses of 50-100 μM SIL-BS were required for significant protection. Apoptosis and interleukin production remained largely unchanged by 10-50 μM SIL-BS but increased slightly after 100 μM treatment, in particular when cells had previously been exposed to 300 µM SM. HaCaT cells, incubated with SIL-BS were lysed and investigated by LC-ESI MS/MS. Findings suggest that SIL-BS is absorbed by HaCaT cells and biotransformed into free silibinin. In summary, silibinin-BS is a promising compound for the treatment of SM injuries: biotransformation to free silibinin is possible and standard doses for clinical use (50-100 µM) provided a significant reduction of necrosis. At doses of 50 µM SIL-BS, no pro-inflammatory or pro-apoptotic effects occurred, but even pro-apoptotic effects of 100 µM SIL-BS were observed only after 300 µM SM exposure and might even be useful to eliminate cells with irreversible SM-induced damage.

Biography:

Guilhem Bousquet is a physician involved in medical oncology since 2005. After his clinical training as a fellowship in Clinical Oncology, he did his PhD thesis in Saint-Louis Hospital in Paris, where he gained an expertise in pathology, xenograft models and pre-clinical pharmacology. He performed a Post-doctoral stay in Pasteur Institute in Lille, and is now Associate Professor in Saint-Louis Hospital and member of the research unit UMR_S1165 University Paris 7/Inserm. His research team is involved in experimental pharmacology and translational research using xenograft models of human fresh tumors. He has published 41 papers.

Abstract:

Therapeutic monoclonal antibodies have widely contributed to improving survival in metastatic cancers. However, patients are at increased risk of developing central nervous system metastases, and the survival of patients with brain metastases remains poor, challenging daily practice in medical oncology. The mechanisms limiting the use of therapeutic monoclonal antibodies for the treatment of brain tumors are their inadequate transport from blood to brain through the blood-brain barrier. We performed a sequential pharmacological pilot study in a young, 36-year-old woman with metastatic breast cancer who developed HER2-overexpressing brain metastases resistant to standard treatment. With her informed consent, lumbar and ventricular reservoirs were implanted for repeated intra-thecal injections of trastuzumab, an anti-HER2 monoclonal antibody. Close monitoring of trastuzumab trough concentrations in the cerebrospinal fluid over 8 months enabled us to determine the intra-thecal drug administration schedule required to stabilize the brain metastases on magnetic resonance imaging. Because of a high clearance from the cerebrospinal fluid, and this result was unexpected, repeated injections of trastuzumab 3 times a week were required. This innovative scheme, guided by individual pharmacology and mimicking a continuous perfusion, can be used for other patients. Apart from this therapeutic effect, the rapid efflux of trastuzumab has not hitherto been described. FcRn receptors, expressed by the capillary endothelium of the blood-brain barrier, may be responsible for this efflux mechanism. Engineering of a F(ab’)2 fragment of humanized monoclonal antibody against HER2 could prevent the binding of immunoglobulin to FcRn, and the mechanism of efflux.

Biography:

Aditya Arya is a Senior Lecturer of Pharmacology at Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. He has received PhD in Pharmacology from the University of Malaya and have published over 30 peer-reviewed papers in reputed Journals. He has been serving as a reviewer for many ISI Journals including editorial board member. His research emphasizes on cellular and molecular Pharmacology, specifically to evaluate the co-relationship between inflammation, cancer and diabetes. He is expert in designing, development and mechanistic prediction of drug molecules on the living system and their role on G-protein-coupled receptors in islet function and stimulus-response coupling in mouse and human islet β-cells. Moreover, to detect and identify novel insulin secretagogues.

Abstract:

The study aimed to investigate the potential role of Rosmarinic acid (RA) in the management of diabetes. RA is an ester of caffeic acid found in various plants which have reflected beneficial effects on different disorders. In our study design, the normal rats were treated with different doses of RA to evaluate acute toxicity. Further on the basis of acute toxicity results, two doses of RA were selected for antidiabetic study on STZ-nicotinamide induced diabetic rats. Diabetic rats were fed 50 and 100 mg/kg body weight of RA daily for 90 days and weekly measured with certain biochemical parameters, blood glucose, insulin, C-peptide, lipid profiles and body weight. At the end of the study period, all the group animals were sacrificed and the blood glucose, insulin, C-peptide, and HbA1c levels were determined in the serum of rats. In addition, histology of pancreas and the expression of glucose transporters (GLUT 1, 2 and 4) proteins were assessed in skeletal muscles and pancreatic tissues. The overall study result demonstrated that RA has potentially normalized the elevated blood glucose levels and significantly improved serum insulin, C-peptide and HbA1c levels thereby reducing cholesterol and bad lipids. Furthermore, the histology result reported recovery in the structural degeneration in the pancreatic tissues, and the western blot analysis showed the significant increase in the GLUT-2 and GLUT-4 protein expression in the skeletal and pancreatic tissues. Altogether, we may postulate that the translocation of glucose transporter proteins (GLUT-4) accelerates the insulin-mediated glucose uptake in muscle and adipose tissue. Thus, we may conclude that RA could be the potential targets for the management of diabetic complications and needs further in depth mechanistic studies at molecular level.

Biography:

Smita Shenoy is an Additional Professor of Pharmacology at Kasturba Medical College, Manipal, India. She has a total of 13 years of teaching experience. She has more than 30 publications in national and international journals.

Abstract:

Serious adverse drug reactions (ADRs) are associated with morbidity and mortality and result in financial burden to the patient and society. A retrospective observational study of serious adverse drug reactions over 1 year in a tertiary care hospital was carried out. Risk factors for serious ADRs were identified (Chi square test). Average direct cost of managing the adverse drug reaction was calculated. Of the 985 adverse drug reactions reported, 95 were serious ADRs. About 49.47% (n= 47) of patients were males and 50.53% (n=48) were females. The mean age of patients with serious ADRs was 48.63±15.59 years. Of the total hospital admissions, 0.05% was due to serious ADRs. The median duration of hospital stay due to serious adverse drug reaction was 7(4, 11) days. Hematological disorders (41.05%) were the most common serious ADRs followed by electrolyte disturbances (18.94%) and hypersensitivity reactions (13.68%).The common serious ADRs were leucopenia (15.78%), febrile neutropenia (12.63%) and hyponatraemia (11.57%). Anticancer drugs constituted the majority of the suspect drugs. Concomitant medications included anticancer drugs, antitubercular drugs, antiretrovirals, antileprotic drugs, antimicrobials, steroids and analgesics. The risk factor for developing serious ADRs was gender (females, p<0.04 versus males), coexisting disease (p< 0.001) and more than two concomitant medications (p< 0.01). The average total direct cost was Rs. 7306.91 per serious ADR. Since ADRs are associated with a wide variety of drugs and can affect any organ in the body, it is important to detect them early and have appropriate preventive strategies.

Biography:

Bharti Chogtu has done MD in Pharmacology. She is Associate Professor in department of Pharmacology. She has published about 45 papers in reputed journals.

Abstract:

Adverse cutaneous reactions to drugs affect about 2-3% of all hospitalized patients. Maculopapular rash is one of the most frequent cutaneous clinical manifestation of non-immediate allergic reactions due to drugs. This study was done to analyze drug induced maculopapular rashes in patients in a tertiary care hospital. It was a prospective study done in patients having maculopapular rashes secondary to drugs for a period of six months. The data was recorded which included demography of the patients, drugs which were implicated in these reactions. The cutaneous adverse drug reactions were then assessed for determining causality and severity. Descriptive statistics was used to analyze the data. A total of 104 patients of drug induced maculopapular rashes were included. The age of the patients ranged from 2-73 years with a median range of 39 years (IQ 21.25-51.75). Males constituted 52.88% of total patients. The most common group of drugs causing maculopapular rash was antimicrobial agents (42.3%) followed by antiepileptics (20%) and non-steroidal anti-inflammatory drugs (14.4%). Of antimicrobial agents, amoxicillin was the most common causative agent followed by antitubercular drugs and nevirapine. Of all the individual drugs, phenytoin was implicated in maximum number (14.4%) of drug reactions. As per WHO causality assessment, 75% of the adverse reactions were possible, 24% probable and 1% certain. The severity of adverse drug reactions was moderate in 85.5% and the remaining reactions were categorized as mild. The offending drug was stopped in 84.6% of patients. 89.4% patients had recovered whereas adverse event continued in the remaining at the time of reporting. Thus, there is a need to monitor cutaneous adverse drug reactions by physicians prescribing antimicrobials and antiepileptics.

Biography:

Shalini Adiga has completed her MD Pharmacologyin the year 2000 from Kasturba Medical College, Manipal, Manipal University. She is the Professor and Head of Pharmacology. She has 27 publications in various journals.

Abstract:

Steven Johnson Syndrome (SJS) is a life threatening muco-cutaneous adverse reaction to medications with high mortality. The aim of this study was to retrospectively review the relationship between drugs induced SJS, the causative agents and the patient characteristics. In patients reported with SJS over a period of 2yrs at a tertiary hospital, data were collected for demographic information, causative drugs, time interval between drug intake and onset of symptoms, duration of hospital stayand clinical outcome. Causality assessment was carried out using the WHO probability scale and data was analysed using SPSS software (version 20).The study included 47 cases of which 29 comprised females. Of the total cases 10 patients were less than 20yrs and 4 patients more than 60 yrs of age with a median age of 40 yrs. Antimicrobials (32%), anti-epileptics (32%) and non-steroidal anti-inflammatory drugs (17%) were the most commonly associated drugs. Amongst antimicrobials fluroquinolones were the most frequent causative drugs followed by cephalosporins and antiretroviral agents. Phenytoin was the commonly implicated antiepileptic drug.The onset of reaction was seen to be most rapid with antibiotics and NSAIDs, with median onset to reaction time being 3 and 4.5 days respectively. Anti-epileptics had the longest latency of 21 days to onset of reaction. Patients developing SJS following antibiotic use had the longest duration of hospital stay, while patients who had no history of drug intake had the least duration (median of 12 days v/s 2.5 days) according to the WHO causality assessment all cases had ‘probable’ association with prior drug intake.

Biography:

Meena Kumari Kamal Kishore has completed her MD in pharmacology from Manipal Academy of Higher Education, currently known as Manipal University. She is an Associate Professor in Pharmacology. She has published more than 30 papers in reputed journals. She is also a moderator for reporting the adverse drug reactions for the pharmacovigilance section of their department. She has also published articles under pharmacovigilance.

Abstract:

Aim: To analyze the hematological adverse drug reactions (ADRs) due to anticancer drugs in a tertiary care hospital. Material & Methods: It was a prospective, observational study done on patients admitted to the medical oncology ward of Kasturba Hospital, Manipal from October 2014 to March 2015. All patients developing hematological adverse drug reactions were included. CDSCO proforma was used for reporting ADRs. Causality was assessed using Naranjo Algorithm. Severity was assessed using Hartwig and Siegel severity scale. Preventability was assessed using Modified Shumock and Thornton preventability scale. Results: Forty patients in this study were found to have hematological ADRs, of which twenty one were males and rest females. Highest incidence was seen in 21-40 y (50%) age group compared to least in 1-20 y (7.5 %) age groups. The most common ADRs were anemia (27.5%), followed by thrombocytopenia (25%), neutropenia (20%), leucopenia (17.5%) and bone marrow suppression (10%). Antimetabolites group contributed to majority of ADRs (30 %), followed by anticancer antibiotics (25%), alkylating agents (15%), topoisomerase-II inhibitors (12.5%), platinum compounds (10 %), microtubule inhibitors (5%) and miscellaneous (2.5%) comprising the least. Totally 24 patients recovered from the ADRs. Majority (97.5 %) of the ADRs were of moderate severity. The results of causality assessment of most of the cases were possible (85 %). All the ADRs were not preventable. Conclusion: Anticancer drugs are known for multiple adverse effects. Early detection and timely management of the ADR with appropriate therapy would reduce the fatal ADRs.

Biography:

Marcela Rizzotto has completed her PhD from Rosario University and Postdoctoral studies from Florianópolis, Barcelona and Sydney University. She teaches at the university in undergraduate and postgraduate courses since many years. She has published more than 25 papers in reputed journals and in more than 100 national and international congresses on topics of antimicrobial metal complexes, chemopreventive action of natural antimutagens, Ames test and Allium test. She heads degree and doctoral thesis and acts as a reviewer in prestigious journals.

Abstract:

DNA is a dynamic molecule that is constantly damaged and repaired. Major sources of DNA lesions are physical and chemical agents from the environment, intermediates of cellular metabolism, spontaneous chemical reactions of DNA, incorporation of foreign or damaged nucleotides, etc. Mutagens are not only involved in genotoxicity and carcinogenesis but also involved in the pathogenesis of several chronic degenerative diseases including hepatic disordes, diabetes, ageing process and so on. One of the best ways to minimize the detrimental effects of mutagens is by the use of natural antimutagens. These include flavonoids, coumarins, carotenoids, tannins and many more.

Biography:

Nilmara de Oliveira Alves is a post-doctoral fellow in the School of Medicine of the University of São Paulo. The researcher, who recently received her doctoral title, focuses on atmospheric pollutants and especially on their effects on health using both in vitro and in vivo tests. For that end, she conducts interdisciplinary projects comprisinggenotoxicity, DNA repair, pathology and atmospheric chemistry.

Abstract:

The Brazilian Amazon population has been negatively affected by biomass burning. The majority of forest fire hotspots in the Amazon take place in the deforestation arcwith a population of over 10 million inhabitants.However, there are few studies to understand the mechanism of action of aerosols in human health. Thus, we collected filters with particulate matter (PM10) to investigate the effects of biomass burning at molecular and cellular levelsusing human lung cells (A549). The chromatography-mass spectrometry analysis showed the presence of carcinogenic and mutagenic compounds. After chemical analysis, we defined a dose below the limit established by the World Health Organization (30 µg/m3). After 24 hours of exposure,there was an increase of pro-inflammatory cytokines and in ROS generation, in a dose and time dependent manner. Besides, there was an induction of cell cycle arrest at G1 phase, as well as an increase in the expression p53 protein and formation of DNA strand breaks. After 72 hours, we detected a significant increase of cells in the sub-G1 fraction, indicating apoptosis. Additionally, we observed the phosphorylation of H2AX (γ-H2AX), which correlated with the activation of caspase 3, suggesting that the induction of γ-H2AXmay be associated with the DNA fragmentation during apoptosis. We also observed that necrosis is a cell demise pathway induced by PM10. This study shows an important advance in understanding the toxic cellular and molecular effects induced by PM10 that can be related to the increase potential of human health impacts in the Amazon region.

Biography:

Ekwere M R is a senior lecturer and a PhD student of Uboh F E. Ekeruke M B is a student under the supervision of Uboh, assisted by Ekwere

Abstract:

The present study evaluated the heamatological parameters of male rats exposed to oral administration of daily doses of 10 mg/ kg and 20 mg/kg uppercott (a mixture of cypermethrin and dimethoate belonging to organophosphate and pyrethroid groups). They were sacrificed after 28 days. Results obtained showed a dose dependent decrease in red blood cell (RBC), packed cell volume (PCV), Mean corpuscular haemoglobin (MCH) and corpuscular heamoglobin concentration (MCHC). White blood cells (WBC), lymphocytes and neutrophils increased significantly (p<0.05) while eosinophiles had no significant change (p>0.05) in concentration comparison with control. Thus, uppercott may induce haematoxicity in mammals.

Biography:

Somnath Paul has completed his PhD dissertation work in 4.5 years, working as graduate student at CSIR-Indian Institute of Chemical Biology since 2010. He is in the process of writing his thesis, to be submitted to Jadavpur University. He has done his Bachelors in Physiology, from Presidency College, Kolkata and Masters in Genetics from University of Calcutta. He has published 7 papers in peer reviewed journals. His major thrust area of research is epigenetics and have future interest in doing research on epigenetic alterations in human diseases and understand the role of epigenetic mechanisms in various patho-physiological outcomes.

Abstract:

Arsenic exposure mainly through drinking water has increased over the years, presently affecting more than 137 million individuals worldwide. One of the prime facets of arsenic toxicity is disruption of epigenetic profile within the cell, leading to various outcomes like silencing or activating genes from their normal state of expression. In the field of toxicology, a recent emphasis lies with the probability of epigenetic alteration and it’s indulgence in DNA damage. Long Interspersed Nuclear Elements (LINE-1) have been studied as a prospective candidate to understand the global genomic methylation profile. Activity and methylation profile of these transposable elements have been associated with various forms of cancers as well as genomic stability. Since arsenic exposure yields a high degree of DNA damage, in our present study we are focusing on the epigenetic risk factor associated with DNA damage and L1-methylation. A total of 100 arsenic exposed samples were recruited from the district of Murshidabad, West Bengal. Cytogenetic damage was analyzed using micronucleus (MN) assay from lymphocytes. When the cohort comparison between arsenic exposed individuals distributed among low, medium and high degree of cytogenetic damage based on the MN frequency, we observed that there was a positive association (p<0.01) between the lowering of methylation profile of LINE-1 with increase in MN frequency. Our data suggests a positive influence of LINE-1 methylation may be related to alteration in chromatin landscape, leading to subsequent genomic instability upon arsenic mediated oxidative DNA damage. LINE-1 methylation hence can be predictive biomarker to epimutagenic events by arsenic.

Biography:

Baragamaarachchi R Y is a first year PhD student who graduated with a first class in BSc Genetics from University of Bangalore. She obtained MSc in Molecular Life Sciences in 2014 from University of Colombo, Sri Lanka. Her research interests lie in Molecular Biology, Immunology, Medicinal plants, Genetics and Microbiology. She has served as a resource person at workshops based on Immunological techniques and awarded at 2nd International Conference on Frontiers in Molecular Life Sciences held in Sri Lanka (2014), for outstanding poster presentation.

Abstract:

Comet assay is a very sophisticated technique use to assess plethora of DNA damages at the level of individual cells and can be applied in a range of fields from human and environmental biomonitoring, routine genotoxicity assessment, DNA repair studies, and clinical studies to molecular epidemiology. Due to its demonstrated advantages and applications it is increasingly acceptable by regulatory authorities as a part of battery of assays used for regulatory submissions in genetic toxicology. Yet the major drawback of this technique is the unreliability in making reproducible data, due to miscellaneous conditions used in different laboratories and due to lack of understanding of the critical steps. Comet assay was performed according to the protocol described by Raymond Tice, with some modifications. Some critical steps that affect the final outcome of the assay were optimized during thisstudy. As the concentration of low melting agarose greatly influenced the comet formation and assay reproducibility, melting of agarose in a boiling water bath was found to be better than melting using a microwave oven. Optimal agarose solidification time was 30 min at 4°C to attain adequately solidified agarose layers which reduce the fragility. Optimal lysis time was 2 h at 4°C. Alkaline unwinding time was increased up to 30 min for adequate denaturation of DNA. The best way to calculate the required voltage to get a voltage drop of 1 V/cm, was to use the spreadsheet developed by Gunnar Brunborg. Electrophoresis for 45 min was found to be sufficient to obtain a considerable DNA migration. However, a small factor, that one would not consider, significantly matters the final outcome and the assay reproducibility.

Biography:

Deniz Özkan Vardar has completed his bachelor’s and master degree at Gazi University. She is PhD student in Department of Nanotechnology and Nanomedicine, Hacettepe University. Her academic work is focused on nanotoxicology especially nano genotoxicology. She has published 2 papers about genotoxicity. She has worked for more than 5 years in the Departments of Health Programs, Hitit University.

Abstract:

Nanomaterials have received enormous attention for their potential applications in biology and medicine. A key issue in evaluating the utility of these materials is the assessment of their potential toxicity−either due to their inherent chemical composition or as a consequence of their nanoscale properties. Quantum dots are an example of a nanomaterial that has been shown to be useful as an alternative to fluorescent dyes for use in biological imaging, due to their bright fluorescence, narrow emission, broad UV excitation, and high photo stability. In addition to labeling of cellular structures in vitro, several groups have demonstrated the use of quantum dots (QDs) for fluorescence imaging in vivo. Several in vitro and in vivo studies have been cited in the literature as demonstrating the lack of evidence for QD-induced cytotoxicity. The sensitivity of the cytotoxicity assay used differs depending on the different mechanisms, which lead to cell death. The MTT assay is simple and rapid to use, which determines, the metabolic activity of the mitochondria can be determined. We aimed to evaluate the cytotoxic effects of silver sulfide quantum dots coated with 2-Mercaptopropionic acid (2MPA) and Meso-2, 3-dimercapto succinic acid (DMSA) because of the lack of studies in this area. Cytotoxicity was evaluated by the MTT assay in HeLa cells. Our results showed that Ag2S QDs were not cytotoxic effects after 24 h exposure.

Biography:

Adetutu Adewale obtained his Ph.D from Department of Biochemistry, Ladoke Akintola University of Technology, Ogbomoso, Nigeria

Abstract:

Background: The development of resistance to currently known conventional anti-malaria drugs has necessitated search into more potent and less toxic anti-malaria drugs of plant origin. Objective: Hence, this study aimed to document plants commonly used to treat malaria in Ilorin metropolis, Nigeria and validate the traditional claims using in vivo anti-plasmodial tests. Methods: Semi-structured questionnaires (70) were used to explore the ethno-botanical practices amongst the traditional healers. The most common species cited were identified, authenticated and their aqueous extracts were screened for antimalarial activities using Plasmodium berghei (NK 65 chloroquine sensitive) and chloroquine as the malarial parasite and positive control respectively. For in vivo anti plasmodial testing, the mice were infected with 1 × 107 parasitized erythrocytes and plant extracts were subsequently administered orally for suppressive, prophylaxis and curative assays. Percentage parasitemia was estimated by standard microscopy and haematological parameters were also measured using standard analyser. Results: Seventy traditional healers from Ilorin metropolis, Nigeria were involved in the study. Forty-three species were recorded with their local names and parts used in the traditional therapeutic preparations. Ten plants with highest frequency of citation (Cymbopogon citrates (17.1%),Azadirachta indica (12.9%), Prosopis africana (12.9%), Vernonia amygdalina(11.4%), Khaya grandifoliola (10%), Terminalia glaucescens (10%), Ziniber officeinale(7.1%), Citrus paradise (7.1%), Parquetina nigrescens (7.1%), Psidium guajava (7.1%),) were selected and investigated for anti-malaria activities. The aqueous extractsof all the selected plants showed significant (p<0.05) anti-malaria activities. P. africana bark extract at 200 mg/kg body weight had the highest chemo-suppressive effect (90.02%) in comparison with other plant extracts and the standard, chloroquine (61.70%) on the 8th day. In addition, the maximum mean survival time (MST) of 23 days were observed in animals administered with P. africana and chloroquine. The extract of P. africana was further analysed for possible bioactive components using Gas Chromatography-Mass Spectrometer (GC-MS). The GC-MS analysis revealed that the aqueous bark extract of P. africana contained lipid (eight), phytochemical (sixteen) and essential oil (eighteen) components. The histological analysis of the liver revealed that the extract of P. africana was able to protect the liver against B. bergei induced damages. Conclusion: Most of the species tested had some antiplasmodial effects, which to some extent supports their traditional inclusion in herbal preparations for treatment of malaria. The bioactive components identified may be responsible for the observed antimalarial activity of P. Africana extract.

Biography:

Shelly Sharma is a research fellow pursuing doctorate from Guru Nanak Dev University, Amritsar, India. She has specialization in the field of Cytogenetics which includes genotoxicity and toxicity of pesticides. She has won Young Scientist Award in an international conference.

Abstract:

Humans are exposed to pesticides and insecticides either directly or indirectly. Exposure to these pesticides may lead to acute toxicity to mammals and non-target organisms. Chlorpyrifos (CPF) is a broad spectrum insecticide widely used in various countries of the world. The aim of the present study was to assess the toxicity associated with chlorpyrifos exposure and possible mitigating effect of cow urine against oxidative stress, activity changes in antioxidant enzymes and inhibition in activity of cholinesterase in rat brain and blood induced by chlorpyrifos. For this purpose LD50 was determined and rats were orally administered with 1/8th of LD50 (19 mg/kg b.wt). Brain and blood samples were taken after 24 hrs, 48 hrs and 72 hrs of treatment. A significant decrease in the activity of AcHE, CAT, SOD and GST was observed along with the increase in MDA levels of both brain and blood in chlorpyrifos treated groups as compared to control. Cow urine treated groups show increase in AChE while decrease in MDA level groups as compared to CPF treated group. The study indicates that cow urine has mitigating effect against toxicity induced by CPF. Thus, it can be used as an antioxidant supplement. Cow urine is considered rich in vitamin A, E and volatile fatty acids which provide antioxidant potential to it.

Biography:

Rajlaxmi Basu aged 27, a graduate student, carrying out her research work at Institute of Haematology and Transfusion Medicine, Medical College, Kolkata, India, for award of PhD degree from University of Calcutta.

Abstract:

Awareness of sewage workers to occupational exposure is growing very slowly in many developing countries due to which they often tend to work without proper protective clothing, resulting in a number of health problems. Lead (Pb) and cadmium (Cd) are present in sewage water and workers are exposed to these metals by unprotected handling during work. These heavy metals exposure are responsible for DNA damage and lowering of blood total iron (Fe) concentration. Zinc (Zn) is a suitable element for promoting metallothionin expression and binds the free cadmium. The total suspended solids (TSS), total dissolved solids (TDS), Pb and Cd were estimated in sewage water. The whole blood Zn and Fe concentration (estimated by energy dispersive X-ray fluorescence), Pd and Cd (estimated by GF AAS) were also estimated. Genotoxicity especially DNA damage was studied by comet assay. It was observed that there are significant differences (p<0.05) of lead and cadmium concentration in blood for exposed population i.e. sewage workers (according to through interview and observation they are non addicted) when compared with control population (non-sewage workers). The DNA damage was also observed to be significantly (p<0.001) higher in exposed groups but their blood iron concentration was significantly lower, which may be the reason for their tendency for retention of blood cadmium and make them more susceptible. Besides, they shows a highly significant depletion (p<0.001) in Selenium (Se) concentration (estimated by energy dispersive X-ray fluorescence) in their whole blood and this may be one of the cause for their lowered antioxidant level and responsible for premature ageing and different other health complication. The higher level of DNA damage (estimated by Single Cell Gel electrophoresis) is also dependent on exposure time and blood heavy metal concentration. The present study also indicates aged workers are rich in blood zinc concentration, which is a suitable indicator as this essential trace element zinc acts as an antidote for the toxic element cadmium. The present study helps to assess the health hazards of sewage workers and more susceptible groups in young compared to aged groups and as per questionnaire and estimation, the young groups have lower blood zinc level as well as different food habits, etc. that may cause DNA damage.

Biography:

Nilmara de Oliveira Alves is a post-doctoral fellow in the School of Medicine of the University of São Paulo. The researcher, who recently received her doctoral title, focuses on atmospheric pollutants and especially on their effects on health using both in vitro and in vivo tests. For that end, she conducts interdisciplinary projects comprising genotoxicity, DNA repair, pathology and atmospheric chemistry.

Abstract:

Atmospheric pollution is an environmental risk factor in large urban centers. São Paulo Metropolitan Area (SPMA), located in the southeast of Brazil, has a population of nearly 20 million people and 8 million vehicles.It is long known that exposure to air pollutants can cause various health effects such as increased inflammatory response and DNA damage. One of the most versatile defense mechanisms against the accumulation of DNA damage is the nucleotide excision repair (NER), which includes the XPC protein.Different studies have shown that knockout mice in the XPC gene have an increased occurrenceof lung tumors.However, the effects of DNA damage caused by air pollutants regarding the lung inflammatory response are largely unknown. In this study, we injected intravenouslyIntercellular Adhesion Molecule-1(anti-ICAM-1) targeted nanoparticles and evaluated the response using IVIS spectrum. Mice were exposed an accumulated dose (concentration vs time of exposure in hours) of 600 µg.m-3during 1 hour, which corresponds to an average concentration of 25 µg.m-3in 24 hours.The next day after exposure, we observeda significantly stronger fluorescent marker for anti-ICAM in the polluted group than the filtered air group. Furthermore, among the animals exposed to ambient pollution, XPC mice have shown a stronger inflammatory response relative to wild mice. The expression of pro-inflammatory cytokines in the lungs is currently being evaluated.These data demonstrate that exposure to ambient air pollution in São Paulo promotes the acute inflammatory responses in mice, especially in knockout mice in the XPC gene.

Biography:

Farhat Naz has completed her PhD in 2014 from All India Institute of Medical Sciences, Delhi in cancer nanomedicine and doing Postdoctoral research in same institute. She is Research Associate in the Dept of Pathology, AIIMS. She has published 3 papers in international journals of repute.

Abstract:

Gold nanoparticles (GNPs) have shown a great potential for use as vehicle for drug delivery and other systemic use. However, long term toxicity remains a major concern. Very few long term in-vivo study pertaining to organ specific biodistribution, sequestration and excretion of GNPs are available. We investigated the long term (90 days) biodistribution, sequestration kinetics, and excretion of ultrafine gold nanoparticles after a single intravenous administration in mice. The sequestration pattern of three different sizes of GNPs 2±0.5 nm, 5±1 nm, and 10±2 nm, at a high dose of 1250 µg/Kg was determined by inductively coupled plasma atomic emission spectrometry (ICP-AES) in various organs such as lungs, liver, spleen, heart, kidney, brain, as well as in blood and urine. GNPs of all three sizes showed highest accumulation in spleen (µg/gm of the tissues) around 15 days after injection and reached near basal level at 90 days. Low concentration of GNPs was detected in brain after 1 day without any residual of GNPs after 30 days. Ultrastructural study also showed few GNPs in brain tissue in lysosome. Renal sequestration was also low indicating reduced nephrotoxic potential. GNPs could be detected in urine till 30 days indicating near total excretion of GNPs following single injection in 1 month. No significant toxicity was documented by normal hemogram, serum biochemistry, and tissue histology. No abnormality was detected in survival, behaviour, skin and hair colour, weight and food intake. Therefore, we concluded that the ultrafine GNPs are mostly excreted out through urine without any systemic toxicity following high dose intravenous administration and it may be safe for systemic use.

Biography:

Baragamaarachchi R Y is a first year PhD student who graduated with a first class in BSc Genetics from University of Bangalore. She obtained MSc in Molecular Life Sciences in 2014 from University of Colombo, Sri Lanka. Her research interests lie in Molecular Biology, Immunology, Medicinal plants, Genetics and Microbiology. She has served as a resource person at workshops based on Immunological techniques and awarded at 2nd International Conference on Frontiers in Molecular Life Sciences held in Sri Lanka (2014), for outstanding poster presentation.

Abstract:

Walidda antidysenterica (Apocynaceae) is widely used in traditional medicinal practices in Sri Lanka and in Asia as a remedy for respiratory disorders, hematuria, spermatorrhoea, chest affections, helminthic disorders, dressing the oozing wounds, jaundice, haemorrhoids, epilepsy, rheumatoid arthritis, osteoporosis, bacterial diseases and gut mobility disorders. Juice extracted from the bark is administrated to treat mouth sores. Flowers are used to treat snake bites, and leaves are used to treat skin disorders such as psoriasis, dermatitis etc. Despite of its medicinal value, it was reported that this plant contain pyrrolizidine alkaloids (a potent toxic compound). Therefore the current study investigated the in vitro toxicity of ethanol leaf, stem bark and flower extracts of W. antidysenterica. The cytotoxic and genotoxic activity of extracts were evaluated against human lymphocytes using trypan blue dye exclusion assay and alkaline comet assay. All extracts exhibited decrease in cell viability (< 70%) at concentrations above 50 µg/ml following 18 hour exposure, except flower extract which retained >80% cell viability even at 1000 µg/ml. Comet assay results indicated that the leaf extract induced DNA damages at the concentrations of 30, 40 and 50 µg/ml (p<0.05) and stem bark extract induced DNA damages at the concentrations of 40 and 50 µg/ml (p<0.05) compared to positive control (H2O2). Flower extract did not induce DNA damages even at 50 µg/ml (p>0.05). In conclusion, the results suggest that the flower extract was neither cytotoxic nor genotoxic whereas leaf extract showed significant cytotoxic and genotoxic activity compared to stem bark extract in a concentration dependent manner.

Biography:

Abstract:

Pesticides are ubiquitous on the planet, and they are employed to control or eliminate a variety of agricultural and household pests that can damage crops and livestock and reduce productivity. Anthropogenic activities are continuously introducing extensive amounts of these compounds into the environment regardless of their persistence, bioaccumulation and toxicity. Despite the many benefits of the use of pesticides in crop production and their significant contribution to the lifestyles we have come to expect, pesticides can also be hazardous if not used appropriately, and many of them may represent potential hazards due to the contamination of food, water and air. However, it is well known that the indiscriminate use of pesticides can generate pest resistance, the emergence of new pest species, environmental pollution, toxic effects, genetic alterations on target and nontarget organisms including humans, and biodiversity loss, among other side effects. Pesticides may be introduced into the aquatic environment since they are applied directly on surface water to control aquatic weeds or via air onto crop fields. Indirect entrance into the freshwater environment is associated with runoff, erosion and lixiviation events resulting from terrestrial application. Furthermore, they may provoke harmful effects on the fish population and other aquatic organisms, e.g., amphibians, contributing to long-term effects in the environment. One of the major goals of our research laboratory is to evaluate the genotoxic and cytotoxic effects exerted by several agrochemicals and their technical formulations on endemic vertebrate Neotropical species, namely Cnesterodon decemmaculatus (Actinopterygii, Poeciliidae) and Rhinella arenarum (Amphibia, Bufonidae) employing several end-points for geno and cytotoxicity. Among them are listed the herbicides dicamba, flurochloridone, glyphosate and 2,4-D.

Biography:

Leon F. Stankowski, Jr., PhD, received BS degrees from The Pennsylvania State University in pre-medicine and biophysics; studied toward a MS in biochemistry at the University of Scranton; and received a PhD in biomedical sciences, specializing in genetics, from the University of Tennessee – Oak Ridge Graduate School of Biomedical Sciences. Since then, he has held various scientific and management positions in contract research organizations and the pharmaceutical industry. He has served a study director for a variety of in vitro and in vivo genetic toxicology assays, and as a program manager or consultant. This latter involves advising clients who have encountered adverse genetic toxicology findings, including the design of custom protocols and mechanistic studies to resolve them. Dr. Stankowski has directed thousands of assays in multiple in vivo and in vitro test systems; has had a lead role in developing and validating novel mutagenesis, in vitro toxicity and biochemistry methods and services; and has published original research results in multiple journals and presented at numerous meetings. He is a member of the Environmental Mutagenesis and Genomics Society and the Genetic Toxicology Association (GTA), and served on the GTA Board of Directors from 2000 to 2003, as the GTA Assistant Treasurer from 2003 to 2006, and as the GTA Treasurer from 2006 to present. He has been a reviewer for several journals in the field, served on numerous industrial workgroups involving in vitro and in vivo mammalian mutagenesis assays, including ASTM, IWGT, US EPA, and ILSI-HESI, and is a US Delegate to the Expert Working Group for the review of most of the OECD Test Guidelines on Genotoxicity.

Abstract:

In vitro genotoxicity assays that are commonly used for regulatory purposes can be categorized into two main groups based upon the endpoints analyzed: gene mutation and chromosome aberration. The single most commonly performed test is the bacterial reverse mutation assay, generally referred to as the Ames assay, which is often used as the first go/no go decision point in product development. Gene mutation can also be evaluated in mammalian cell test systems, such as the mouse lymphoma or CHO/HPRT assays, where the cells become resistant to metabolic poisons after loss of specific gene function. The other main group of assays is based upon cytogenetic analyses that examine changes in chromosome structure or number. Clastogens induce structural changes that can be detected microscopically and may manifest as breaks or rearrangements involving one or both chromatids of one chromosome, or multiple chromosomes. While chromosome aberration assays may detect limited types of numerical aberrations (polyploidy and endoreduplication), the micronucleus assay is better suited for that purpose since it can detect aneugens (spindle poisons) that cause more limited changes in chromosome number (i.e., gain or loss of single chromosomes). The basic principles underlying these assays and their basic design will be presented, as well as a discussion of the pros and cons of each.

Biography:

Rohan Kulkarni is currently serving as the Director of Genetic Toxicology-Study Management at BioReliance. Rohan received B.Sc. degree in Zoology from Mumbai University, in 1998 and M.Sc. degree in Zoology and Marine Science from Mumbai University in 2000. Before relocating to the US in 2003, he worked as a Product Development Specialist at TechnoSource, a start-up Biotech company in India. He received his Ph.D. from Wayne State University, MI in Biological Sciences in 2008 under Dr. James D. Tucker. He received the Prestigious Alexander Hollander Travel award in 2003 at the 38th EMS Meeting in Atlanta. Dr. Kulkarni completed his postdoctoral fellowship from National Center for Toxicological Research, US FDA in 2011 in the Division of Genetic and Molecular Toxicology. He joined BioReliance in October 2011 as a Senior Scientist for in vivo and in vitro cytogenetic assays at BioReliance, with Study Director Responsibilities for GLP and non-GLP cytogenetic studies. In 2015, he was appointed as the Director of Genetic Toxicology-Study Management. He has presented much of this work in several book chapters, poster presentations and many journal articles. Dr. Kulkarni is a full member of Society of Toxicology, Genetic Toxicology Association and an Associate Member in the American College of Toxicology. He is also a member of the Genetic Toxicology Technical Committee organized by the ILSI-HESI group and a member of the Core committee for In vivo follow-up testing.

Abstract:

In vivo genetic toxicology testing is performed usually in rodents such as rats or mice to determine the potential of DNA damage that can affect chromosomal structure or mitotic apparatus such as spindle fibers that in turn could changes chromosome number. In vivo assays can also detect genotoxic agents missed in in vitro tests. These assays are mainly divided into two broad categories; either to detect chromosome damage or DNA damage. The positive result of induced chromosomal damage is an increase in frequency of micronucleated PCEs or increase in chromosome aberrations. Micronucleus is a small nucleus that forms whenever a chromosome or a fragment of a chromosome is not incorporated into one of the daughter nuclei during cell division. This is typically caused by loss of chromosomal fragments due to clastogenicity or loss of entire chromosome due to spindle fiber malfunction as a result of aneugenicity. The mammalian in vivo chromosome aberration test is used for the detection of structural chromosome aberrations in bone marrow. The in vivo alkaline single cell gel electrophoresis assay, also called alkaline Comet Assay is a method measuring DNA damage. This Assay can be used to detect DNA damage caused by double strand breaks, single strand breaks, alkali labile sites, oxidative base damage, and DNA cross-linking with DNA or protein. The basic principles underlying these assays and their basic design will be presented along with the regulatory guidelines governing these assays.

Biography:

Marcelo L. Larramendy was born in La Plata, Argentina and obtained his Ph.D. at the Faculty of Natural Sciences and Museum from the National University of La Plata (UNLP), Argentina, in 1978. Appointed Member of the Research Career of the National Scientific and Technological Council of Scientific and Technical Research of Argentina (CONICET) in 1981, coating today as SeniorResearcher. Since 1991,he serves as Professor of Molecular Cell Biology at the UNLP. Former Member of the Executive Committee of the Latin American Association of Environmental Mutagensis, Teratogenesis and Carcinogenesis (ALAMCTA). Author of more than 450 contributions in the field, including scientific publications, mostly in high impact and prestigious scientific journals, research communications and conferences worldwide. Lecturer at many conferences and courses worldwide. Recipient of several national and international awards including, among others, the \"Bernardo Houssay 1987\" and the \"Diamond Cover Award 1992\" granted by CONICET, Argentina and the American National Society for Histotechnology (USA). Prof. Dr. Larramendy is a regular Lecturer at the international A. Hollaender Courses organized by the International Association of the Environmental Society (IAEMS). He has carried out post-Doctoral research activities at the National Cancer Institute (NIH), Bethesda, USA and has been Guest Scientist at the Department of Medical Genetics at the University of Helsinki, Finland. Expert in Molecular Cytogenetics, Genetic Toxicology and Ecotoxicology. He is, or has been, referee for more than 20 international scientific journals including some of the top periodicals within his scope of work. Editor of eight books in his field which have been widely acknowledged internationally. Member of the International Panel of Experts at the International Agency for Research on Cancer (IARC, WHO, Lyon, France) in 2015 for the evaluation of DDT, 2,4-D and Lindane. Presently, Prof. Dr. Larramendy is Head of the Laboratory of Molecular Cytogenetics and Genotoxicology at the UNLP, a multidisciplinary research team which includes researchers, research students and staff, keeping strong collaborative links with several Argentinean and international research groups as well as the industry.

Abstract:

Pesticides are ubiquitous on the planet, and they are employed to control or eliminate a variety of agricultural and household pests that can damage crops and livestock and reduce productivity. Anthropogenic activities are continuously introducing extensive amounts of these compounds into the environment regardless of their persistence, bioaccumulation and toxicity. Despite the many benefits of the use of pesticides in crop production and their significant contribution to the lifestyles we have come to expect, pesticides can also be hazardous if not used appropriately, and many of them may represent potential hazards due to the contamination of food, water and air. However, it is well known that the indiscriminate use of pesticides can generate pest resistance, the emergence of new pest species, environmental pollution, toxic effects, genetic alterations on target and nontarget organisms including humans, and biodiversity loss, among other side effects. Pesticides may be introduced into the aquatic environment since they are applied directly on surface water to control aquatic weeds or via air onto crop fields. Indirect entrance into the freshwater environment is associated with runoff, erosion and lixiviation events resulting from terrestrial application. Furthermore, they may provoke harmful effects on the fish population and other aquatic organisms, e.g., amphibians, contributing to long-term effects in the environment. One of the major goals of our research laboratory is to evaluate the genotoxic and cytotoxic effects exerted by several agrochemicals and their technical formulations on endemic vertebrate Neotropical species, namely Cnesterodon decemmaculatus (Actinopterygii, Poeciliidae) and Rhinella arenarum (Amphibia, Bufonidae) employing several end-points for geno and cytotoxicity. Among them are listed the herbicides dicamba, flurochloridone, glyphosate and 2,4-D.

Biography:

Kamala Pant is Principal Scientist and study director for various genetic toxicology assays at BioReliance. She received her master’s degree in physical chemistry from Agra University, India. She has more than thirty five years of experience in conducting and directing different mutation and DNA damage assays. Kamala has represented Bioreliance in several international Validation and Guideline development Programs such as, European Centre for Validation of Alternative Methods (ECVAM) - SHE Cell Transformation assay, Japanese Center for Validation of Alternative Methods (JaCVAM) - comet assay, New Energy and Industrial Technology Development Organization, Japan (NEDO) project - Bhas Cell Transformation Assay and OECD guideline program for genetic toxicology with emphasis on in-vivo comet and cell transformation assays. She has been involved in the International Working Group on Genetic Toxicology (IWGT) for comet assay. She has been a long time member of the Genetic Toxicology Association (GTA) and has served as a member of the Board of the GTA.

Abstract:

In drug development, genotoxicity testing is an essential part of preclinical safety evaluation. Before a potential drug candidate is selected, many chemicals have to go through pre-screening in drug discovery/lead optimization to weed out any “bad actors”. Non-GLP assays used at early stages to select candidates for further development as they have lower cost, quick turn-around time, minimal test article requirement. However, these assays should be predictive of the standard GLP assays. For impurities that are not feasible to isolate or synthesize or when compound quantity is limited, it may not be possible to achieve the highest test concentrations recommended for an ICH-compliant bacterial mutagenicity assay according to the current testing guidelines. In this case, bacterial mutagenicity testing could be carried out using a miniaturized assay format with proven high concordance to the ICH-compliant assay to enable testing at higher concentrations with justification. Virtually any regulatory assay can be scaled down to conserve test article, time and money by using fewer dose levels, replicates, strains or animals. Also in some cases fewer cells are scored. For Ames assay, modifications of the standard assays (e. g. 24-well, 6 well methods) or different techniques with good predictive qualities (e.g. Ames II assay with liquid format) are available. For cytogenetics assay, modified designs with either reduced scoring or reduced culture size are offered. Different designs and the pros and cons of these design modifications will be discussed during the workshop.

Biography:

Roberts has a MS in Biotechnology from Johns Hopkins University and is currently a Ph.D. candidate in the Joint Graduate Toxicology Program at the Environmental and Occupational Health Sciences Institute at Rutgers University. He started his genetic toxicology career at Litron Laboratories by assisting with flow cytometric micronucleus kit development while learning how to conduct and direct bacterial reverse mutation assays. Mr. Roberts started a flow cytometry lab at Covance Laboratories, Inc., and as a Research Associate in the Genetic and Molecular Toxicology Department, he supported the development of multiple assays including aneugenicity detection, using CREST antibodies and pan centromeric probes, and the flow cytometric rat Pig-a gene mutation assay, to phenotypically evaluate in vivo gene mutation. Currently, he is a Research Scientist in the Genetic Toxicology Department of Bristol-Myers Squibb and is responsible for conducting and supporting non-clinical safety studies to ensure worker and patient safety. Mr. Roberts is presently serving a 3-year term as a board of director for the Genetic Toxicology Association and was nominated to be the 2016 Chair of the organization. He is actively interested in developing new genetic toxicity assays for hazard identification purposes, with focus on utilizing newer technologies like next generation sequencing to advance the science of genetic toxicology.

Abstract:

The purpose of genotoxicity assays are to prevent human exposure to potential carcinogens. Carcinogenicity testing is not conducted until the last phases of drug development and genotoxicity assays are used as surrogates to predict their outcome by measuring initial key events in the carcinogenic process. During lead optimization, screening assays are used to assist in selection of a drug candidate lacking significant safety hazards. These screening assays include; computerized assessment for the presence of structural features known to represent mutagenic hazards, bacterial reverse-mutation assays (Ames tests), in vitro mammalian cell assays, and appropriate animal studies. Once identified, drug candidates progress to full development where more extensive genotoxicity testing is conducted in compliance with formalized regulatory guidelines. A positive outcome in any of the in vitro assays triggers follow-up testing in vivo to better understand the biological relevance of the positive finding. Ideally, in vivo follow-up testing is conducted using integrated study designs where genotoxicity endpoints are added on to general toxicology studies. This creates a powerful data set as drug exposure levels, organ toxicity, histopathology, clinical pathology, body weights, and clinical observations are obtained concomitantly with genotoxicity endpoints from each biological replicate. This presentation will summarize pathways for enabling first in human drug studies and discuss strategies for developing new chemical entities that are mutagenic, clastogenic, aneugenic, or contain genotoxic impurities.

Biography:

Michael Fasullo earned his PhD at Stanford University School of Medicine, Department of Biochemistry, and completed his Postdoctoral studies at Columbia University in the field of DNA repair and recombination. He has published over 25 papers in the field of DNA damage response, radiation repair and environmental toxicology. His current interest centers on high throughput screening for resistance to P450-activated carcinogens. He is currently an Associate Professor at the State University of New York Polytechnic Institute, Albany, NY.

Abstract:

The human response to environmental carcinogens that require bioactivation is highly variable. Environment, lifestyle, and genetics are factors that influence bioactivation. Genetic factors include polymorphic P450 and DNA repair genes; however, epidemiological studies may lack significance due to inadequate patient numbers. We used budding yeast as a model organism to determine genetic susceptibility to food-associated carcinogens, including benzopyrene (BaP), aflatoxins (AFB1) and heterocyclic aromatic amines (HAAs). Budding yeast does not contain P450s that activate these compounds, so we introduced expression vectors that contain specific human P450 and NAT2 genes. In yeast, either CYP1A2 or CYP1A1 activates AFB1, while both CYP1A2 and NAT2 are required for activation of IQ. To measure genotoxic effects, we measured recombination and mutation frequencies, Rad51 foci, growth inhibition and DNA adducts, as in a previous publication concerning CYP1A2 polymorphisms. Here, we analyzed two CYP1A1 polymorphisms, T461N and I462V, correlated with breast and lung cancer. Although some studies have suggested that these polymorphisms confer reduced activity, both CYP1A1 polymorphisms are highly efficient at activating the AFB1and benzo[a]pyrene dihydrodiol (BaP-DHD). To determine resistance genes, we used a high throughput approach for screening the yeast deletion library expressing specific P450 genes. Screens for aflatoxin resistance identified checkpoint and RNA metabolism genes that are mutated in cancers. We are now performing screens to identify genes involved in resistance to 2-amino-3-methylimidazo [4,5-f] quinoline (IQ). Preliminary data identified both recombinational repair and DNA damage tolerance genes. Further high throughput analysis will be performed using other food carcinogens, including 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) and 2-amino-3,8- dimethylimidazo [4,5-f] quinoxaline (MeIQx).

Biography:

Silma Pereira completed her PhD in Biological Sciences (Genetics) from the University of São Paulo, Brazil (2000) and post-doctoral level at Georgetown University Medical Center in Washington, D.C., USA (2010). She has experience in Human Genetics, with emphasis in: molecular cytogenetics, genetics of infectious diseases and mutagenesis. She coordinates the Laboratory of Genetics and Molecular Biology at Federal University of Maranhão (Brazil). She has published more than 25 papers in scientific journals and has been a reviewer in the fields of human genetics, epidemiology and genetic toxicology.

Abstract:

Leishmaniasis is a neglected tropical infection, considered the third most important vector-borne disease. Facing the strong prevalence among large populations in the world, the World Health Organization recommends treatment based on pentavalent antimonials as first-choice drugs, such as Glucantime® (meglumine antimoniate). Nevertheless, its structure, mechanisms of action and mutagenic properties are not fully elucidated. Our group has demonstrated that Glucantime® induces DNA damage in vivo, but not in vitro. We suggest that this drug is a pro-mutagenic compound that causes damage to DNA after reduction from the pentavalent antimony (SbV) into the more toxic trivalent antimony (SbIII). Our findings also include isoflavones protective effect, specially ginistein, a potent antioxidant, reducing Glucantime® genotoxicity. In this sense, we analyzed DNA damage score by COMET assay using the FPG (formamidopyrimidine DNA – glycosylase) that removes apurinic sites or products as 8OHdG originated by the guanine oxidation. Our data showed an increase of the damage score when compared to the conventional COMET assay. This reinforces the hypothesis that oxidative stress is one of the mechanisms of the drug’s action. Our current investigation aims to analyze the differential expression of genes involved in oxidative stress on infected animals, as well as determine the parasite load in animals treated with Glucantime® and genistein concomitantly. Therefore, the discovery of this mechanism is important for the development of therapeutic strategies and new approaches that aim to reduce the side effects of Glucantime® without affecting its efficacy on leishmaniasis treatment.

Biography:

Arpiné has received a Diploma degree in chemistry from the Lebanese University of Beirut, Lebanon in 2008. She then shifted her academic focus towards pharmacokinetics in Mediterranean University of Marseille, France in 2009. She began her Ph.D. thesis in neurotoxicology at the University of Saarbrücken, Germany and University of Lorraine of Metz, France under Pr. Alexandra K. Kiemer and Pr. Rachid Soulimani. Her thesis focused on the evaluation of the short and long term neurotoxic effects following lactational exposure to the sum of the six non-dioxin-like polychlorinated biphenyls at low levels in offspring mice. Arpiné was awarded her Ph.D. in 2012 and continued her post-doc in University of Lorraine, Metz/Nancy, France in early 2013. Her current research focuses on the mechanisms of action and developmental neurotoxicity testing of chemicals at low environmental exposure.

Abstract:

We have previously shown neurobiological changes and developmental/behavioral performances in mice exposed during lactation to a representative environmental mixture of the six indicator non-dioxin-like polychlorinated biphenyls (∑6 NDL-PCBs) at low levels. In this study, we analyzed the global gene expression profile in cerebellar neurons isolated from male mice presenting the most significant induction of anxiety-like behavior in our previous study (10 ng/kg ∑6 NDL-PCBs). Our results revealed an up regulation in the expression of genes belonging to GO terms involved with the cell cycle, DNA replication, cell cycle checkpoint, response to DNA damage stimulus, regulation of RNA biosynthetic processes, and microtubule cytoskeleton organization. Down regulated genes belonged to terms involved with the transmission of nerve impulses, projection neurons, synapse hands, cell junctions, and regulation of RNA biosynthetic processes. Using qPCR, we quantified gene expression related to DNA damage and validated the transcriptomic study, as a significant over expression of Atm, Atr, Bard1, Brca2, Fancd2, Figf, Mycn, p53 and Rad51 was observed between groups. Finally, using immunoblots, we found significant changes in the protein expression of Atm, Brca1, p53, Kcnma1, Npy4r and Scn1a between exposed and control groups, indicating that the expression pattern of these proteins agreed with the expression pattern of their genes by qPCR, further validating our transcriptomic findings. In conclusion, our study showed that early life exposure of male mice to a low level of ∑6 NDL-PCBs induced p53-dependent responses to cellular stress and a decrease in the expression of proteins involved in the generation, conduction, and transmission of electrical signals in neurons.

Biography:

Marcela Rizzotto has completed her PhD from Rosario University and Postdoctoral studies from Florianópolis, Barcelona and Sydney University. She teaches at the university in undergraduate and postgraduate courses since many years. She has published more than 25 papers in reputed journals and in more than 100 national and international congresses on topics of antimicrobial metal complexes, chemopreventive action of natural antimutagens, Ames test and Allium test. She heads degree and doctoral thesis and acts as a reviewer in prestigious journals.

Abstract:

DNA damage is a critical factor in carcinogenesis. Human exposure to endogenously formed N-nitroso compounds is related to an increased risk of gastric, esophageal, nasopharyngeal and bladder cancer. Endogenous nitrosation occurs in the stomach between amine and amide precursors and nitrite. Sulfonamides, which are widely used for their various properties (antimicrobial, antidiabetic, herbicides, analytical reagents, etc.), are potentially nitrosatable due to its amine and/or amide functions. Previously we found mutagenicity in reaction mixtures formed by selected sulfonamide and nitrite, so, we began to study the antimutagenic activity of L-ascorbic acid (AA) and green tea extracts on the acute toxicity and mutagenicity of these reaction mixtures by means of the Allium and Ames tests and by electronic spectroscopic analysis.
Conclusions 1. AA and green tea infusion showed a high ability to inhibit the direct mutagenicity of reaction mixtures sulfonamide-nitrite (tested sulfonamides: sodium sulfathiazole, complex cobalt (III)-sulfathiazole), either added before or after the nitrite, at pH 1-2. 2. By the Allium test it was found that not genotoxic substances are produced by interacting of AA with such mixtures sulfonamide-nitrite. 3. No direct mutagenicity was observed in the glibenclamide-nitrite system in the Ames test. This system showed the same microscopic behavior that glibenclamide with the Allium test. The UV-Vis spectra allow to check that there is no reaction between the said sulfonylurea and nitrite in the experimental conditions. 4. For all the above, both AA and green tea infusions are presented as effective anti mutagens to mitigate the mutagenicity of mixtures sulfonamide-nitrite in acidic media.

Biography:

G Wultsch studied Medicine at Medical University of Graz. He has completed his PhD at the age of 25 years from Graz Medical University and conducted Postdoctoral studies as well in the Medical University of Graz Medical University of Graz. He is the Chief Medical Officer of the Occupational Medical Center in Graz and the Head of the occupational medicine branch of the Austrian medical chamber. His work combines the control of the health status of the employees in various industries as well as the function as a consultant to various chambers. The results were published in 7 articles in reputed journals (one is accepted for publication in Mutat Res – Reviews, and the results of 2 investigations are in preparation).

Abstract:

Exfoliated cells can be collected with non-invasive methods from different organs. It is possible to analyze nuclear aberrations which provide information about genotoxic and acute cytotoxic effects caused by exposures. Genotoxic effects lead to formation of micronuclei (MNi), nuclear buds and binucleates while acute cytotoxic effects lead to formation of pyknosis, condensed chromatin, karyorrhexis and karyolysis. Recently, a standardized protocol was developed for experiments with buccal cells and the scoring criteria can be also used for nasal cells. Several studies were conducted in which the impact of life-style exposures was investigated in these cells. Clear-cut positive effects were detected in mouth cells of heavy smokers. Furthermore, the finding indicates that MNi formation increases with exposure to tar while unexpectedly an inverse association with nicotine uptake was observed. Also khat and betel chewing led to increased MNi rates in buccal cells while coca chewing caused a protective effect. In total ca. 80 occupational studies were conducted so far with exfoliated nasal and buccal cells. Results of investigation in Austria show that significant MNi induction is detectable in nasal but not in buccal cells of welders, while in wood workers only a baseline effect was detected in both cell types. Consistently negative results were obtained in electroplaters and in workers which were exposed to chicken manure. However, evidence of acute cytotoxic effects was observed in all aforementioned studies. Overall, the findings indicate that cytome assays with exfoliated cells are a valuable tool to detect heath risks caused by exposure to genotoxins.

Biography:

Rutao Liu has completed his PhD from Shandong University and Postdoctoral studies from Albert Einstein College of Medicine, Yeshiva University. He is the Director of China - America CRC for Environment & Health of Shandong Province. He has published more than 120 papers in reputed journals and has been serving as an Editor of Advances in Environmental Protection.

Abstract:

Lead toxicity has been proved to be related with inducing oxidative stress of organisms, and causing inactivation of antioxidant enzymes, the mechanism of which remains unknown. This study investigated and compared superoxide dismutase (Cu/Zn SOD) activity inhibited in lead-treated zebrafish livers and explored the mechanism of SOD inactivation by lead at the molecular level using multiple spectroscopic techniques, isothermal titration calorimetric (ITC) measurement, molecular docking study and ICP-AES detection. Results showed lead exposure decreased SOD activities in zebrafish livers due to direct interactions between lead and SOD, resulting in conformational and functional changes of the enzyme. To be specific, Studies at the molecular level indicated that lead bound into the active site channel of SOD, hindered the path of the catalytic substrate (O2-•), damaged its skeleton conformation and secondary structure, and interacted with the enzymatically related residue (Arg 141) through electrostatic forces (ΔH<0, ΔS>0), and caused the release of Cu2+ and Zn2+ from the catalytic pocket of SOD. This work shows a correlation between results on organismal and molecular levels, and obtains a possible model hypothesizing mechanisms of lead toxicity using in vitro experiments instead of in vivo ones.

Biography:

Syamantak Mani Tripathi is an Assistant Professor in the Department of Veterinary Pharmacology and Toxicology, College of Veterinary Science and Animal Husbandry, Chhattisharh Kamdhenu Vishwavidalya, Durg-491001 (Chhattisgarh) India. He has over six years experience with hand-on applications including teams of researchers and technicians in the Pharmacology & Toxicology and Biotechnology division. His training and experience also includes applied animal investigation skills as a research scholar in the field of pesticide induced immunotoxicology and safety pharmacology studies. He has worked in multiple successful research projects funded by Indian Council of Agricultural Research and Department of Biotechnology, Government of India, supporting clinical development and leading to strong regulatory submissions for pesticides uses in agriculture. His research program is focused on the study of immune response to pesticide and xenobiotics in avian model. He received his Bachelor’s in Veterinary Science and Animal Husbandry from Jawaharlal Nehru Krishi Vishwavidyalaya, Jabalpur (MP), India; Master’s of Veterinary Pharmacology from Anand Agricultural University, Anand (Gujarat), India and his Ph.D. in Veterinary Pharmacology and Toxicology from the Nanaji Deshmukh Veterinary Science University at Jabalpur (MP), India. His academic work was focused on “Immuno-genotoxicity of organophosphorous insecticide ‘acephate’ in white leghorn birds”. His work contributes towards understanding the molecular mechanism of acephate toxicity in avian model; studying interleukin gene(s) associated with immunity and development of test series to study immunotoxicity. Memberships he has include the Indian Society of Toxicology, Indian Society of Veterinary Pharmacology and Toxicology.

Abstract:

Acephate, widely used insecticide in agriculture, is a common environmental contaminant. Although health effects of the acephate are documented, however developmental immuno toxic studies are scanty and need more attention. Medicinal plants, since times immemorial, have been used virtually in all cultures as a source of medicine for altering the immune systems. A group of medicinal plant including Apamarg (Achyranthes aspera) and Bhui Amla (Phyllanthus niruri) growing in India were examined for their immunomodulatory effect in White Leghorn cockerels. The present study was undertaken in day-old white leghorn cockerels to assess immuno toxicity for sub chronic exposure to acephate. The chicks were divided into nine groups. Groups C1 and C2 served as plain control and vehicle control respectively. Chicks of groups T1, T2 and T3 were administered acephate suspended in groundnut oil at 21.3 mg/kg, 28.4 mg/kg and 42.6 mg/kg respectively orally for up to 60 days. Chicks of groups T1+Aa, T2+Aa, T3+Aa, T1+Pn, T2+Pn and T3+Pn were administered acephate together with extract of two medicinal plants A. aspera and P. niruri extract suspended in groundnut oil at 21.3 mg/kg+Aa (1ml), 28.4 mg/kg+Aa (1ml) and 42.6 mg/kg+Aa (1ml), 21.3 mg/kg+Pn (1ml), 28.4 mg/kg+Pn (1ml) and 42.6 mg/kg+ Pn (1ml) respectively orally for 60 days. All the chicks were vaccinated with Ranikhet disease virus (F-strain; RD-F) on days 1 and 30. During the course of study and at term, parameters of cellular and humoral immunity were determined. The live body weight gain, absolute and the relative weights of spleen, thymus and bursa of Fabricius, antibody response to RDF, delayed type hypersensitivity response to 2,4-dinitro-1-chlorobenzene or PHA-P were significantly reduced in the medium and extremely toxic treatment groups. The ability of lymphocytes proliferation in response to antigen RD-F and mitogen Con A was also significantly suppressed following subchronic exposure to acephate. Furthermore, histopathologically, bursa and spleen showed mild depletion of lymphocytes. No significant alteration in the live body weight gain, absolute and the relative weights of spleen, thymus and bursa of Fabricius, antibody response to RDF, delayed type hypersensitivity response to 2,4-dinitro-1-chlorobenzene or PHA-P, the ability of lymphocytes proliferation in response to antigen RD-F and mitogen Con A and histopathology of bursa and spleen were observed in the birds concurrently exposed to acephate and A. aspera and P. niruri. Therefore, immuno toxicological effects should be considered when assessing the acephate risk to human and animal health. It was concluded that sub chronic acephate exposure at low concentrations may affect immune responses in avian species. Furthermore, the immuno toxicity induced by acephate could be efficiently ameliorated by A. aspera and P. niruri.

Biography:

K S Tilak is a Doctorate from Andhra University, Waltair, AP, India, the former Dean of faculty of Natural Sciences, Chairman Board of Studies (PG) Zoology and Head of the Department of Zoology and Aquaculture having 40 years of research experience in the field of “Aquatic Toxicology”, having guided 29 research degrees, published 72 research papers in international and national journals recipient of prestigious ‘Archana Gold Medal’ by Academy of Environmental Biology, editor and reviewer of reputed journals, attended and conducted international and national conference in Acharya Nagarjuna University, India.

Abstract:

Genotoxicity is the property possessed by organisms and due to various carcinogens in which some are mutagens causing defects even in natal stage. The effects are attempted in two modes acute or chronic, resulting the products of oxidative damage especially in human urine and finally reflect the overall damage to all tissues and organs in the body. The chronic levels manifest changes in biochemical parameters and such sub-lethal effects at biochemical level viz: acetylcholinesterases (ACh), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-s-transferase (GSH), alkaline phosphatase (ALP), aminotransferases (SGOT & SGPT), and malonialdehyde (MDA). Erythrocyte AChE was significantly decreased in farmer/sprayers at the instant of exposure and the decrement recorded as 45% and 36% respectively in RBC and plasma. A sampling data were analyzed as three separate, target, exposed and control groups characterized by time scale exposure differing in age and smoking habits, symptomatic and asymptomatic group consisting of nicotinic and muscarinic class and finally methylated and ethylated op and mixed also. Similary SOD, CAT, GPx, Transaminase’s ALP lipid per oxidation and GSH activities resulted different changes in the pesticide exposed exposure. The studies of genotoxicity in humans reflect the influence of the body’s metabolic activation and detoxification systems. Comets form as the broken ends of the negatively charged DNA molecule become free to migrate in the electric environment towards the anode. Micronuclei are formed when acentric chromatid or chromosomal fragments, fail to migrate towards the spindle poles, and are not incorporated into the daughter nuclei. 8-hydroxydeoxyguanosine is a ubiquitous marker of oxidative stress and is an oxidatively modified guanosine which is also mostly frequently detected DNA lesion in urine. The pesticide exposed workers had higher levels of DNA by tail DNA as percentage, Olive Tail Movement (OTM) and tail length and age group; the exposed workers had significantly more DNA damage. The micronucleus (MN) analysis showed significantly higher MN induction in the smokers both in the control as well as in the exposed group resulting higher frequencies. The increased urinary levels of 8-OHdG were contributed by both non-smokers as well as smokers in the exposed groups.

Biography:

Kim Strifert was previously employed as a healthcare administrator at the Mayo Clinic, the Department of Obstetrics and Gynecology and the Office of Academic Analytic Support at Baylor College of Medicine. She is currently affiliated with the Graduate School, School of Public Health, at the University of Alabama at Birmingham. Her recent article \"The link between oral contraceptive use and the increase in the prevalence of autism spectrum disorder\" is available through the Elsevier Journal Medical Hypotheses. The article is of significance to all women and their families as it hypothesizes that the increase in the occurrence of autism coincides with the increase in the use of hormonal contraceptives. It is important because it identifies the lack of medical research into the neuro developmental effects of oral contraceptive use on offspring and calls for further research.

Abstract:

It is now estimated that 1 in 68 children are diagnosed with ASD in the United States. So far, no definitive cause or contributing factors have been established to account for the increase in prevalence in ASD. Combined oral contraceptive (COC) use is one possible risk factor for the increase in prevalence that has been overlooked in the existing biomedical and epidemiologic literature. One of the compounds found in combined oral contraceptives (COCs) is the synthetic estrogen Ethinylestradiol (EE2). EE2 is a known endocrine disrupting compound (EDC) capable of causing harmful effects to the endocrine system and to progeny. Since COCs were developed to mimic natural human hormones and disrupt endogenous endocrine function to prevent pregnancy, there is reason for concern that the EE2 component may be associated with the adverse neurodevelopmental effects that lead to the increase in ASDs. This hypothesis is compelling due to several considerations. As the prevalence of COC use has risen over the last fifty years so has the prevalence of ASDs. As a category of agents there are specific documented mechanisms through which COCs can affect the oocyte and/or developing embryo. As COCs are taken deliberately, exposure occurs at pharmacologically effective concentrations. The possibility exists that the effects of COC use could intensify over generations due to transgenerational transmission of altered epigenetic programming, with continued exposure across generations imparting sensitivity to developing ASDs. Lastly, the specific demographic at risk, women who are likely to have children, is the exact demographic that is taking COCs.

Biography:

Michael B Morgan completed his PhD at Georgia Institute of Technology. His Postdoctoral training included a position as a Postdoctoral fellow at Georgia Tech followed by a position as a Postdoctoral Associate at Georgia State University. He is currently an Associate Professor of Biology at Berry College. His research interests are in stress responses of aquatic invertebrates. Specifically he investigates how cnidarians respond to various types of anthropogenic stressors. His molecular expertise is in using differential gene expression techniques to detect, isolate, and characterize gene transcripts expressed from corals experiencing stress.

Abstract:

Cnidarians do not have endocrine organs; however they are capable of responding to signaling molecules such as hormones. Endocrine disruption has been suspected in cnidarians but no direct hormone interaction has been identified. Regulatory pathways associated with hormone bio synthesis and signaling are essentially uncharacterized in cnidarians. Representational Difference Analysis (RDA) is a differential gene expression technique that can successfully be applied to cnidarians experiencing stress. The objective of this study was to isolate transcripts that were responsive to a sublethal exposure of estradiol. The sea anemone Exaiptasia pallida was exposed to 20 µg/l estradiol for four hours. Results identify transcripts that appear to have functional significance related to steroid exposure. Results presented also demonstrate how small labs with limited financial resources can use RDA coupled with Quantitative Real-Time PCR (qPCR) to perform transcriptional analyses in hypothesis driven experiments to identify potentially important biomarkers of stressor-specific exposures. Conclusions will discuss how human pharmaceuticals through sewage treatment effluent are representative of a class of anthropogenic stressors capable of impacting aquatic invertebrates.

Biography:

Qingcheng Mao is an Associate Professor of Pharmaceutics at the University of Washington, Seattle, Washington. He received his PhD in Biochemistry from the University of Berne in Switzerland, and completed Postdoctoral training at the University of North Carolina and Queen’s University in Canada before joining the faculty of the University of Washington in 2002. His research mainly focuses on mechanistic understanding and prediction of drug/xenobiotic disposition during pregnancy including fetal exposure to drugs and xenobiotics. He has published over 50 peer-reviewed papers and has been serving as an Editorial Board Member for “Drug Metabolism and Disposition”.

Abstract:

Glyburide is commonly prescribed for the treatment of gestational diabetes mellitus; however, fetal exposure to glyburide is not well understood and may have short- and long-term consequences for the health of the child. Glyburide can cross the placenta; fetal concentrations at term are nearly comparable to maternal levels. Whether or not glyburide is metabolized in the fetus and by what mechanisms has yet to be determined. In this study, we determined the kinetic parameters for glyburide depletion by CYP3A is oenzymes; characterized glyburide metabolism by human fetal liver tissues collected during the first or early second trimester of pregnancy; and identified the major enzyme responsible for glyburide metabolism in human fetal livers. CYP3A4 had the highest metabolic capacity towards glyburide, followed by CYP3A7 and CYP3A5 (Clint,u = 37.1, 13.0, and 8.7 ml/min/nmol P450, respectively). M5 was the predominant metabolite generated by CYP3A7 and human fetal liver microsomes (HFLMs) with approximately 96% relative abundance. M5 was also the dominant metabolite generated by CYP3A4, CYP3A5, and adult liver microsomes; however, M1-M4 were also present, with up to 15% relative abundance. CYP3A7 protein levels in HFLMs were highly correlated with glyburide Clint, 16α-OH DHEA formation, and 4′-OH midazolam formation. Likewise, glyburide Clint¬ was highly correlated with 16α-OH DHEA formation. Fetal demographics as well as CYP3A5 and CYP3A7 genotype did not alter CYP3A7 protein levels or glyburide Clint. These results indicate that human fetal livers metabolize glyburide predominantly to M5 and that CYP3A7 is the major enzyme responsible for glyburide metabolism in human fetal livers.

Biography:

Mary M Staehle is an Assistant Professor of Chemical and Biomedical Engineering at Rowan University. Before joining the faculty at Rowan in 2010, she worked at the Daniel Baugh Institute for Functional Genomics and Computational Biology at Thomas Jefferson University and received her PhD in chemical engineering from the University of Delaware. She also holds a BS in Biomedical Engineering from the Johns Hopkins University. Her research interests include neuro regenerative dynamics, the characterization of toxicity in novel materials, systems biology, and biomedical control systems.

Abstract:

Schmidtea mediterranea (Smed) planaria are small, freshwater flatworms with a centralized nervous system, a sequenced genome, and a large population of pluripotent stem-like cells known as neoblasts. These worms have remarkable regenerative capabilities, including the ability to regenerate any or all of the nervous system. We hypothesize that head regeneration in Smed is analogous to neurodevelopment in higher level organisms like humans and that these processes require similar mechanisms such that characterization of the disruption of head regeneration in Smed provides insight into neurodevelopmental effects in humans. We have tested this hypothesis with exposure to two known teratogens: ethanol and bisphenol A (BPA). Our results indicate that the reacquisition of cognitive function in head-regenerating Smed exposed to either of these is delayed, as evidenced by delayed movement-normalized photophobic behaviour. This suggests direct effects on neuro regenerative processes that can be characterized at the molecular level. We have also begun to use this system to assess BPA-alternative materials. Taken together, our results suggest that the Smed could be a “coal-mine canary” for neurodevelopmental effects of novel materials.

Biography:

P Sampath Kumar has completed his UG and PG in Medicine from University of Madras, India. He has more than two decades of experience in Forensic Medicine & Toxicology consultation at Sri Ramachandra University, Madras. For the past 15 years, he has been working as a Professor and Head and Vice-Principal of this institute. He is also the President of Medico Legal Society of Tamil Nadu, Chennai. He is also the Member of Advisor Committee of IXth Annual Conference of Indian Society of Toxicology to be held in August 2015 at Chennai.

Abstract:

For a patient, doctor is equivalent to God and the God is infallible. But that is for patients. In reality, doctors are human beings and to err is human. Combined drug intoxication (CDI), also known as multiple drug intake (MDI) is an unnatural cause of human death. CDI is confused with drug overdose, but it is a different phenomenon. The reasons for toxicity vary depending on the mixture of drugs. Most victims die after using certain combinations that suppress breathing, lowers blood oxygen level and causes brain death. These include mixtures of over-the-counter the drugs, legally or illegally obtained prescription drugs, herbal mixtures, and home remedies. Ingestion of alcoholic beverages, in combination with other drugs, increases the risk of CDI. Analgesics, antihypertensive, multivitamins are the common drugs which are used in CDI. Easy availability of these drugs has resulted in their abuse. Antihypertensive drugs constitute leading form of cardiovascular drug overdose. Among these calcium-channel blockers and beta blockers take the lead. Toxicity with these drugs causes refractory bradycardia, hypotension, pulmonary edema and cardiac arrest which are a great challenge for any treating physician. This article is presenting a case of a 19 year old college student with alleged history of multiple-drug intake of amlodipine, atenalol, and aspirin with ethyl alcohol. The patient treated initially in a tertiary care center casualty, failed to respond to treatment. He was shifted to a multidisciplinary coronary care unit wherein he was given treatment using state of the art facilities and he survived.

Biography:

T G Borovskaya has graduated from the Tomsk State Medical University got Doctoral degree and completed her Postdoctoral studies from the Goldberg Research Institute of Pharmacology. She is the Head of Laboratory of Pharmacology. She has published 3 monographs, more than 160 papers in reputed journals and is the author of 14 patents. Her field of interests covers toxicology, andrology and embryology.

Abstract:

At present there are oncologic diseases that are considered to be fundamentally curable, but with chemotherapeutic agents only. Effectiveness of treatment of these patients includes keeping their reproductive function actual. The aim of this work was to study experimentally the reproductive status of female rats depending on cytostatic impact of drugs. The objective also included a comparative assessment of toxic effects of anti-neoblastoma agents on posterity, as well as investigating the ways of pharmacological correction of pathological changes in posterity. Platidiam, carboplatin, epirubicin, etoposide, paclitaxel were administered to female rats in a maximally tolerated dose. It was obtained that the earliest menopause can be expected after administration of anthracycline antibiotic. Fertility was significantly decreased after application of second-generation platinum compound and inhibitor of topo-isomerase activity. The largest number of pathological changes in viable posterity was observed after administration of paclitaxel. Among the drugs correction of posterity the uromitexan, glutoxim and kortagen are considered.

Biography:

Patrícia Pereira, after her PhD, was awarded a grant for Post-doctoral research from the Portuguese Science Foundation (FCT) and she established fruitful research collaborations like those successfully achieved in 3 recent FCT projects. She is the sole aquatic toxicologist being part of the Portuguese team for polar research. She has published 37 papers in international journals with referees, 1 book chapter and 3 conference papers. She has presented 45 communications (35% in oral format).

Abstract:

Eyes have a central role in the perception of the surrounding medium and in maintaining organisms’ homeostasis. Mercury (Hg) (including methylmercury - MeHg) is a ubiquitous contaminant of natural waters and a potent neurotoxicant that affects visual functions but few studies concerning to wild fish are available. This study contributes to fill this knowledge gap by the evaluation of Hg accumulation in the eye wall of wild grey mullet (Liza aurata) together with the assessment of biochemical endpoints related with the oxidative stress status and neurotransmission. This approach was complemented by the characterization of environmental contamination profiles (both in water and sediment). Sampling was conducted in two sites of a Portuguese coastal lagoon (Aveiro lagoon): (i) Largo do Laranjo (LAR) located in an Hg contaminated confined area, and (ii) São Jacinto (SJ) closer to the lagoon inlet and selected as reference site. Winter and summer conditions were considered. Eye wall was analysed for total Hg (tHg) and methylmercury (MeHg) levels, as well as for antioxidant responses (CAT, SOD, GPx, GR, GST), peroxidative damage and acetylcholinesterase (AChE). Inorganic mercury levels (iHg) were estimated by the difference between tHg and MeHg levels. tHg, iHg and MeHg in eye wall were higher at LAR than SJ in winter and summer, reflecting environmental spatial differences of water column and surface sediments. Moreover, fish caught at LAR in winter showed a significant decrease of CAT and SOD, in line with the occurrence of peroxidative damage. A different spatial pattern was recorded for those biological endpoints in summer, being characterised by the increment of GR and GPx at LAR, eventually preventing the occurrence of lipid peroxidation. Additionally, AChE was enhanced at LAR in summer pointing out an interference with the cholinergic system. The PCA analysis allowed discerning a cause-effect relationship between accumulated iHg and MeHg with GPx and LPO, particularly at LAR. Current data pointed out the vulnerability of fish eyes to environmental contamination by Hg. This neurotoxicant can be accumulated in eye wall leading to alterations in the cellular protection against oxidative stress. Such repercussions could eventually compromise fish visual capacity.

Biography:

Suhera M. Aburawi has completed her Ph.D at Cairo University (1999), and M. Phill at London Hospital Medical College (1984). She has published more than 23 papers in reputed journals, and contributed to more than 24 conference papers. She was invited, by several journals, to review submitted manuscripts. She also contributed the chapter on Libya in several editions of D’Vanzo, C.E. and Geissler, E.M. (eds.), Cultural Health Assessment, Mosby Inc.

Abstract:

Introduction: Infertility is a source of psychological and sometimes social stress on parents who desire to have children. Formaldehyde is used chiefly as disinfectant, preservative and in the chemical synthesis. The medical uses of formaldehyde are limited, but focused especially on laboratory use. Selenium is an essential trace of mineral element for human; it is essential for sperm function and male fertility. Selenium deficiency has been linked to reproductive problems in animals. Objectives: To investigate the prophylactic and curative effect of selenium on male infertility induced by formaldehyde using male albino mice. Method: Forty male albino mice were used, weight 25-30gm. Five groups of male mice (n=8) were used. Group 1 was daily administered water for injection (5ml/kg) for five days, group 2 was daily administered selenium (100 μg/kg) for five days, group 3 was daily administered formaldehyde (30mg/kg) for five days, group 4 (prophylaxis) was daily administered a combination of formaldehyde and selenium for five days, while group 5 (curative) was daily administered formaldehyde for five days followed by daily administration of selenium for the next five days. Intraperitoneal administration was adopted. At the end of administration, seminal fluid was collected from vas deferens. Sperm count, morphology and motility were scored; Histopathological screening of genital system was carried out. SPSS software was applied for comparing groups. Results & Conclusion: It was found that formaldehyde toxicity did not change the sperm count and percentage of motile sperm; unhealthy sperm was increased, while healthy sperm was decreased. Formaldehyde produces degeneration/damage to the male mice genital system. Selenium alone produces an increase in sperm count, volume of seminal fluid and the percentage of motile sperm. Selenium has prophylactic and curative effects against formaldehyde-induce genital system toxicity. Future work is recommended to find out if selenium protective effect is through antioxidant or other mechanisms.

Biography:

Adamma A. Emejulu Completed her PhD in 2012 from the Federal University of Technology, Owerri (FUTO) Nigeria, where she is a lecturer and researcher in the Department of Biochemistry. She has up to 18 publications in both local and international reputed journals to her credit. She is an officer of the Organization for Women in Science for the Developing World, FUTO chapter.

Abstract:

Renal and hepato-protective effect of Irvingia gabonensis juice on sodium fluoride-induced toxicity in wistar rats: Twenty-four male albino rats divided into 4 groups of 6 animals each and all, except normal control(NC), were intoxicated with 20mgKg-1body weight of sodium fluoride(NaF) daily by gavage for 35 days. Sodium fluoride control group(NaFC) received only the toxicant. Test group(IG) received I. gabonensis juice concurrently with the toxicant, while the standard control(Q + Vit. E) received concurrently,15mgK-1 body weight Quercetin + 100 mgK-1 bodyweight α-tocopherol throughout the 35 days. Normal control(NC) received only standard pelletized diet and water. Serum aspartate aminotransferase(AST), alanine aminotransferase(ALT), total protein, albumin, total cholesterol, serum creatinine and electrolyte levels were assayed among test, standard and control animals. Irvingia gabonensis significantly(p < 0.05) reduced AST activity in the IG group (137.68 ± 12.66 U/L) compared to NaFC group (175.12±10.63 U/L). This compares to the reduction in the standard(Q+ Vit. E) group(135.69 ± 10.66 U/L). ALT activity was also reduced in the IG group. Effect of I . gabonensis on albumin and cholesterol levels were similar to that of the standard group. Administration of I.gabonensis also significantly (p<0.002) reduced elevated creatinine and Cl- concentrations, while significantly (p<0.05) elevating serum Ca2+ and Mg2+ ion levels. I.gabonensis fruit juice has some renal and hepato -protective potential which may be due to the presence of secondary plant metabolites like flavonoids, tannins and alkaloids found in the plant. The fruit is also rich in Ca2+ and Mg2+ . Increased domestication is encouraged.

Biography:

Diana Anderson holds the Established Chair in Biomedical Sciences at the University of Bradford. She obtained her first degree in the University of Wales and second degrees in the Faculty of Medicine, University of Manchester. She has over 450 peer-reviewed papers, 8 books, has successfully supervised 26 PhDs, and been a member of editorial boards of 10 international journals. She has been or is Editor in Chief of a book Series on toxicology for J.Wiley and sons and the Royal Society of Chemistry respectively. She gives key note addresses at various international meetings. She is a consultant for many international organisations, such as the WHO, NATO, TWAS, UNIDO and the OECD

Abstract:

The food mutagens IQ (2-amino-3-methylimidazo[4,5-f]quinoline) and PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine) are heterocyclic amines (HCA), generated when heating proteinaceous food. This study investigates the protective potential of the flavonoids quercetin (Q) and rutin (R) against oxidative stress induced in vitro by IQ and PhIP in lymphocytes from healthy individuals and untreated, newly diagnosed colon cancer patients using the Comet assay. In the presence of up to 500 μM Q and R, the DNA damage resulting from a high dose of PhIP (75 μM) or IQ (150 μM) was significantly reduced (P < 0.001) to levels comparable to six times lower IQ or 7.5 times lower PhIP doses. Lymphocytes from colon cancer patients had greater baseline DNA damage than those from healthy individuals (P < 0.01) and this higher level of damage was also observed throughout in vitro treatment. Except for the >50 years of age group and male gender, confounding factors such as smoking, drinking and/or dietary habits were not found to be significant. In conclusion, flavonoids reduced oxidative stress caused by food mutagens in vitroin lymphocytes of healthy individuals and colon cancer patients. Thus, dietary supplementation with flavonoid-rich vegetables and fruits may prove very effective in protecting against oxidative stress.

Biography:

Balszuweit F is a pharmacist and obtained his PhD at the Free University Berlin in 2005. Along with his research activities within the Bundeswehr Medical Service, he has been concerned with research management, regulatory affairs and scientific cooperation. His research interests are focused on cell co-cultures to identify novel treatment strategies, in particular against sulfur mustard injuries.

Abstract:

Sulfur Mustard (SM) is a chemical warfare agent, causing skin blistering, inflammation and impaired wound healing. Due to its complex effects, no causative antidote has been established despite decades of medical research. Advanced cell culture studies may provide new insights to significantly improve future therapeutic options. HaCaT cells, immortalized keratinocytes were co-cultivated with THP-1 (a monocyte-derived cell line) and exposed to SM. 2% THP-1, similar to ratio of resident immune cells in human skin in vivo, resulted in a strong increase of necrosis, apoptosis and inflammation after SM exposure. Further increase of THP-1 concentrations had little additional effects. It was, thus, demonstrated that immune cells, when exposed to SM have an aggravating effect on SM toxicity. Co-culture of HaCaT with 2% THP-1 takes the effect of immune cells into account, is a closer approximation of in vivo conditions and thus a more valid test system, compared to HaCaT monocultures. Anti-inflammatory compounds, including dexamethasone and two NSAIDs (ibuprofen and diclofenac) were tested, both in HaCaT monocultures and HaCaT-THP-1 co-culture after SM exposure. Dexamethasone had some protective effects in the monocultures, but these effects were less pronounced in co-cultures. In contrast, diclofenac, having shown only negligible effects in monocultures demonstrated highly protective effects in co-cultures. Ibuprofen however, had aggravating effects on SM toxicity in monocultures and these effects even worse in co-cultures. In summary, our results demonstrate that effects of immune cells have to be taken into consideration when studying SM toxicity in cell cultures. Use of HaCaT-THP-1 co-culture can provide new insight into efficacy and safety of potential antidotes.

Biography:

Lenita de Freitas Tallarico is a Biologist and Professor whose scientific fields of study are ecotoxicology and malacology. She completed her PhD from Nuclear Energy Research Institute (University of São Paulo) and Postdoctoral from State University of Campinas and Butantan Institute. Her current area of investigation is focused on the molecular and morphological phylogeny of mollusks, reproduction, bioindicators and environmental monitoring.

Abstract:

Chemical compounds in the aquatic environmental can cause effects on organisms, interacting with natural stressors, affecting the reproduction and survival of the exposed population. It is important to consider the new tools for understand the relationship between the levels of contaminants in the ecosystem and their effects on the local biota. For this, the best strategy is to use native species with ecological significance and sensitive to environmental pollutants. Considering that two thirds of the Earth is compound by aquatic environment and more than 90% of the living species are invertebrates and that gather the second largest group in kingdom Animalia, the mollusks represent an important group in food chains. These organisms are vital to sustaining many habitats, and have been excellent environmental health indicators, acting as early warning sentinels of habitat deterioration. Tests developed with molluscan species may therefore be more amenable to extrapolation in risk assessment programs than ones based on phyla less numerically significant. Several studies demonstrated that freshwater gastropods have been important in eco toxicological assessments, especially with Biomphalaria glabrata (Say, 1818), Lymnaea stagnalis (Linnaeus, 1758) and Potamopyrgus antipodarum (Gray, 1843). The development of new toxicity and mutagenicity tests with species of environmental significance is necessary for the adoption of control profiles in polluted areas and serves to conserve areas less disturbed. The next step that being started is standardize these assays by regulatory agencies to evaluation of the chemical substances and water samples.

Biography:

Alenka Franko, Associate Professor, MD, is a specialist in occupational medicine at the Clinical Institute of Occupational Medicine, University Medical Centre, Ljubljana, Slovenia. Her research and teachings focus on several themes: Occupational and environmental toxicology, molecular epidemiology, genetics and gene-environment interactions, occupational medicine. She carries out work in these areas nationally and internationally. She has been a speaker at many national and international conferences.

Abstract:

It has become increasingly obvious that both environmental and genetic factors may influence the development of many diseases. Genes coding for enzymes that are involved in the metabolism of foreign chemical substances have mostly been primary candidates for gene-environment interactions studies. This study investigated the influence of gene-gene and gene-environment interactions on the risk of developing asbestosis. The study comprised 262 cases with asbestosis and 265 controls with no asbestos-related disease previously studied for MnSOD, ECSOD, CAT, GSTT1, GSTM1, GSTP1, and iNOS polymorphisms. Data on cumulative asbestos exposure and smoking were available for all subjects. PCR-based methods were used to genotype MnSOD Ala –9Val, ECSOD Arg213Gly, CAT –262C>T, iNOS (CCTTT)n, GSTM1-null, GSTT1-null, GSTP1 Ile105Val and Ala114Val polymorphisms. To assess gene-gene and gene-environmental interactions, logistic regression was used. The analysis showed that the associations between MnSOD Ala–9Val polymorphism and the risk of asbestosis as well as between iNOS genotypes and asbestosis were modified by CAT –262 C>T polymorphism (p=0.038; p=0.031). A strong interaction was found between GSTM1-null polymorphism and smoking (p=0.007), iNOS (CCTTT)n polymorphism and smoking (p=0.054) as well as between iNOS (CCTTT)n polymorphism and cumulative asbestos exposure (p=0.037). The findings of this study suggest that the interactions between different genotypes, genotypes and smoking, as well as between genotypes and asbestos exposure have an important influence on the development of asbestosis and should be considered seriously in future research on occupational/ environmental asbestos-related diseases.

Biography:

Ying Peng has completed his PhD at the age of 31 years old from School of Medicine, Sun Yat-Sen University, Guangzhou, China and finished his Postdoctoral training in National Cancer Institute- at Frederick, NIH, MD, USA. He is a Director and Professor of Department of Neurology, Sun Yat-Sen Memorial Hospital, SunYat-Sen University. As a clinical neurologist, he has published 88 papers in reputed journals and is serving as an Associate-Editor-in-Chief of “Chinese Journal of Nervous and Mental Disease”. He is the Deputy-Chief of Neuro-pharmacological Association of Guangdong province, and Deputy-Chief of Neurological division of Doctor Association of Guangdong province, China.

Abstract:

Morphine abuse in treating chronic pain has become a worldwide problem. But repeated morphine exposure can cause memory impairment with its mechanisms not fully elucidated by current researches. Autophagy is an important pathway for cells to maintain survival. Here we show that repeated morphine injection in C57BL/6 mice for 7 days activates autophagic flux mainly in the hippocampi, with subsequent spatial memory impairment confirmed by Morris water maze test. Autophagy inhibition by 3-methyladenine aggravates memory impairment induced by morphine and is correlated with increased cellular apoptosis in the hippocampus. Furthermore, we show morphine suppresses the expression of TNF-α, IL-6 and iNOS, and inhibition of autophagy up-regulates the expression of TNF-α, IL-1β, IL-6 and iNOS, as well as NF-kappaB’s activation. Taken together, our data indicates that autophagy canal leviate the memory impairment caused by morphine through inflammation suppression in hippocampi of C57BL/6 mice.

Biography:

F Balszuweit is a pharmacist and obtained his PhD at the Free University Berlin in 2005. Along with his research activities within the Bundeswehr Medical Service, he has been concerned with research management, regulatory affairs and scientific cooperation. His research interests are focused on cell co-cultures to identify novel treatment strategies, in particular against sulfur mustard injuries.

Abstract:

Sulfur mustard (SM) is a vesicating chemical warfare agent causing skin blistering, ulceration, impaired wound healing, prolonged hospitalization and permanent lesions. Silibinin, the lead compound from Silybum marianum, has been discussed as a potential antidote to SM poisoning, but previous investigations had been limited to nitrogen mustards. Water solubility of silibinin is poor, thus a water-soluble prodrug, e.g. silibinin-bis-succinat (silibinin-BS, SIL-BS) should be desirable for rapid bioavailability as an antidote. HaCaT cells were exposed to SM (30, 100, and 300 μM) for 30 min and treated thereafter with SIL-BS (10, 50, and 100 μM) for 24 h. Necrosis, apoptosis and production interleukin-6 and -8 were determined. SIL-BS dose-dependently reduced SM cytotoxicity, even after 300 μM exposure. Doses of 50-100 μM SIL-BS were required for significant protection. Apoptosis and interleukin production remained largely unchanged by 10-50 μM SIL-BS but increased slightly after 100 μM treatment, in particular when cells had previously been exposed to 300 μM SM. HaCaT cells, incubated with SIL-BS were lysed and investigated by LC-ESI MS/MS. Findings suggest that SIL-BS is absorbed by HaCaT cells and biotransformed into free silibinin. In summary, silibinin-BS is a promising compound for the treatment of SM injuries: biotransformation to free silibinin is possible and standard doses for clinical use (50-100 μM) provided a significant reduction of necrosis. At doses of 50 μM SIL-BS, no pro-inflammatory or pro-apoptotic effects occurred, but even proapoptotic effects of 100 μM SIL-BS were observed only after 300 μM SM exposure and might even be useful to eliminate cells with irreversible SM-induced damage.

Biography:

Shou-Lin Wang has completed his PhD in 2006 from Nanjing Medical University (NMU), China, and postdoctoral studies from Rutgers University School of Public Health. He is the Head and Professor of Department of Occupational Medicine and Environmental Health, NMU. He has published more than 100 papers in reputed journals and got several scientific awards in China.

Abstract:

The study aims to illustrate the association of 2,2’4,4’-tetrabromodiphenyl ether (BDE47) with diabetes in a two-stage case-control study and animal experiment. All the participants received a questionnaire, health examination, and the detection of 7 PBDE congeners in serum. Then, male rats were exposed to BDE47 for 8 weeks to explore its effects on glucose homeostasis, and potential mechanisms using high-throughput genomic analysis. Detection rate of serum ∑PBDEs in cases was significantly higher than controls, which presented a higher risk in the 3rd tertile of ∑PBDEs, particularly in Study II (OR=2.32, ptrend=0.031). Among the 7 congeners, BDE47 showed significant high detection rate and concentration in cases in both two studies and their combination. Every tertile of BDE47 significantly increased the risk of diabetes, particularly in Study II (ptrend=0.006) and the combined study (ptrend=0.002). Animal experiments confirmed that BDE47 treatments induced hyperglycemia in male rats. Furthermore, gene microarray analysis showed that type 1 diabetes (T1D) pathways and three gene ontology (GO) terms involved in glucose transport were enriched. The study first demonstrated that environmental exposure to BDE47 might increase the risk of diabetes through activation of T1D pathways and upregulation of genes involved in glucose transport.

Biography:

Heba Youssef Sayed has completed MD in Clinical Toxicology from Faculty of Medicine Ain Shams University, Cairo Egypt in 2005 and Postdoctoral studies from ASU School of Medicine. She was the initiator of Medical Crisis Management Unit Faculty of Medicine ASU from 2011-2013. Currently she is the vice dean for community services and environmental development affair Faculty of Medicine Port Said University since November 2014. She has published more than 18 papers in reputed journals at national and international levels.

Abstract:

Introduction: Several studies indicated that monosodium glutamate (MSG) disrupts the metabolism, the development, and the functions of various organs, such as liver, thymus, ovaries, kidney, and many parts of brain, including cerebellum. Nitric Oxide (NO) is known to be responsible for the organization of many biological events in the mammalian body as a second messenger and a neural messenger. Some studies found that NO is a neuroprotective substance while others qualify it as a neurotoxic. Aim: This study was designed to investigate the effect of non-selective inhibition of nitric oxide synthase enzyme isoforms on cerebellar structure and function in normal rats and in rats with MSG-induced cerebellar toxicity. Materials & Methods: The study groups included thirty two SD rats which were divided into 4 groups; control, LNAME-treated, MSG- treated and LNAME+MSG-treated groups. Motor coordination was assessed by rotarod test. Cerebellar nitrite concentration was measured. Histopathological evaluation of cerebellar structure and immunohistochemical examination for caspase-3 were done. Results: Both LNAME and MSG treatments significantly impaired cerebellar function and resulted in marked cerebellar injury and an increase in apoptosis. This effect was most prominent with combined treatment with LNAME and MSG. Conclusion: Current study results suggest that NO has a neuroprotective role in the cerebellum as inhibitionof nitric oxide synthase enzyme impaired cerebellar function in normal rats and accentuated MSG-induced cerebellar toxicity.

Biography:

Olujimi O O is an emerging researcher and a lecturer in the Department of Environmental Management and Toxicology, Federal University of Agriculture, Abeokuta, Ogun State, Nigeria. He recently completed his PhD at Cape Peninsula University of Technology, Cape Town on the determination and health risk assessment of Endocrine Disrupting Chemicals (Phthalates, phenols and heavy metals) in freshwater systems of Cape Town Environment. He has over 7 years of teaching and research experience with over 30 publications as book chapters, peer-reviewed journals and conference proceedings.

Abstract:

Phthalate esters (PEs) are ubiquitous organic pollutants that have been found to possess endocrine disrupting potential. This study assessed the levels of PEs in influent and effluent from Covenant Oxidation Pond (COP) and Ikeja Wastewater Treatment Plant (IWWTP) and the efficiencies of the two treatment processes at removing PEs congeners. Water samples were collected using amber bottles, acidified and stored at 4°C prior to extraction. The potential health risk arising from the usage of effluent-polluted river water as well as the physical and chemical characteristics of water samples were determined using standard methods. Liquid-liquid extraction method followed by column clean-up and Gas Chromatography-Flame Ionization Detector (GC-FID) were employed for the determination of the PEs. The mean values for physical and chemical parameters analyzed in samples from the two processes ranged from 7.1 to 7.5 for pH, 30.1°C to 30.5°C for temperature, 0.97 to 5.01 mgL-1, 118 to 302 mgL-1, 249 to 556 mgL-1 and 522 to 794 μScm-1 for Dissolved Oxygen, Biochemical Oxygen Demand, Chemical Oxygen Demand and Electrical Conductivity, respectively. The pH and temperature ranges were within the WHO acceptable limits while DO, BOD, COD and EC were above the limits. Monomethylphthalate, Dimethylphthalate, Diallylphthalate, Diethylphthalate, Diisobutylphthalate, Butylbenzylphthalate, Din- butylphthalate and Di-(2-ethylhexyl) phthalate were present in all the samples. The monthly mean concentrations varied between 1.63 (Diisobutylphthalate) and 46.9 μgL-1 (Di-(2-ethylhexyl) phthalate) in influent and between 0.64 (Diallylphthalate) and 38.9 μgL- 1 (Di-(2-ethylhexyl) phthalate) in effluent at COP and from 2.33 (Diisobutylphthalate) to 40.6 μgL-1 (Di-(2-ethylhexyl) phthalate) in influent and 0.81 (DAP) to 27.8 μgL-1 (DEHP) in effluent at IWWTP. The mean removal efficiency of PEs at IWWTP was higher (54%) than COP (43.3%) during the study period. The health risk assessment of PEs did not suggest non-cancer effects in adults and children as values varied from 3.42x10-4 (DAP) to 0.138 (DEHP) at COP and from 4.32x10-4 (DAP) to 9.8x10-2 (DEHP) at IWWTP. However, communities downstream may be exposed to potential carcinogenic effects as values obtained for adults and children ranged from 2.39 x 10-7 (DAP) to 3.84x10-5 (DEHP) at COP and from 3.02x10-7 (DAP) to 2.74x10-5 (DEHP) at IWWTP. Dermal absorption route may pose more carcinogenic risk than ingestion of effluent-polluted water.

Biography:

Sharda Shah Peshin’s area of interest is Toxicology and Poisoning. She has a number of research publications in toxicology and poisoning including research papers, books, manuals, brochures and management cards. She has also published a number of educative leaflets, posters and handouts to raise awareness about the safe use of chemicals and prevention of poisoning. This literature is of immense help to hospitals, primary health centers and general public. She was a member of the Protocol Development Group of the National Snakebite Management Protocol India, Directorate General of Health Services, Ministry of Health & Family Welfare, Govt. of India, 2008.

Abstract:

Indiscriminate and unsafe use of different chemicals in the form of pesticides, household products, drugs, industrial chemicals etc has led to an increasing incidence of accidental and intentional poisoning, resulting in morbidity and mortality. To determine the incidence and trend of poisoning due to various agents over a period of five years (Apr.2009-Mar. 2014), we analyzed the data of the telephonic consultations by treating physicians, to the National Poisons Information Centre, from different parts of India. The substances commonly involved in poisoning were classified into eight groups’ viz household products, agricultural pesticides, industrial chemicals, drugs, bites and stings, plants, unknown and miscellaneous classes. Age ranged from < 1yr - 70yrs.Data in children were divided into four age groups (Gp.I: 0-6yrs.,Gp.II: >6-12yrs.,Gp.III : >12-16yrs.,Gp.IV :>16-18 yrs.).The Centre received a total of 8958 calls during the five year period, with 94.77% calls on management of poisoning and 5.22% seeking information about various products and functioning of the Centre. Males outnumbered females (M=62.14%, F=37.85%). Mode of poisoning was predominantly unintentional (58.61%) followed by intentional mode (39.70%). The common routes of exposure were oral (94.86%) dermal (3.6%),inhalation, (0.9%) and ocular routes(0.4%) respectively. The household products were most commonly implicated (45.04%) with highest number of calls due to pesticides(16.64%) followed by detergents and corrosives (14.40%). Drugs (22.15%) mainly comprised of benzodiazepines, analgesics and anticonvulsants. Amongst the agricultural pesticides (16.14%) organophosphates, aluminium phosphide and pyrethroids were commonly implicated. Industrial chemicals (7.71%) chiefly included copper sulfate. Bites and stings (2.99%) comprised mainly snake bites and plants(2.34%) paticularly involved Dhatura. Calls due to unknown and miscellaneous products were few (1.55%, 2.04%). A striking feature of the study was a high incidence of poisoning in children (51.76%) with Gr.I being most affected (71.66%).The exact magnitude of poisoning in the country is not known because the data is scattered. The Poisons Centre data also may not be a true reflection of the scenario in India because a large number of calls are never reported to the Centre. However, the results of the present study highlight an increasing use of household products and their misuse. Easy accessibility and careless storage coupled with negligible parental supervision in case of children could be the possible reasons for poisoning. The study stresses the need to identify high risk circumstances, susceptible age groups, common products and environmental toxins involved in poisoning and implementation of prevention programmes in order to reduce morbidity and mortality.

Biography:

S S Hundal, Professor of Zoology, completed his PhD from the Punjab Agricultural University, Ludhiana, India. He has a distinguished career in teaching, research and outreach activities. His main research interests are effect of environmental contaminants on animal physiology and on bioconversion of agricultural wastes. He has supervised 9 MSc and 2 PhD students. He has published more than 50 research papers; attended as resource person and invited speaker at more than 35 national and international conferences and seminars. He is Reviewer for four international journals and serving on the Editorial Board of two journals.

Abstract:

The concept of stress in an organism that results in an internal physiological response in living organisms has been recognized and hypothesized to involve important adaptive changes that are necessary to restore homeostasis. Different conditions produce similar stress responses, and the ability of organisms to adapt to stress is regulated by the integration of the nervous, immune and endocrine systems; mediated by hormones and is ultimately played out at the level of cells and molecules. Stress plays a prominent role in cellular aging because the cells have to withstand and respond to major types of stress in their environment, including genotoxic and oxidative stress often leading to initiating a cell death program. Oxidative stress occurs when highly reactive molecules - free radicals - overwhelm the cell’s natural defenses against their attack. Under conditions of oxidative stress, cellular machinery fails and eventually impairs function by slowing down physiological processes. The different types of pollutants released to environment in every moment by the human activity enter different ecosystems from different pathways - industrial wastes, human disposal, toxic chemicals, sewages, radio nuclides, organic pollutants, air and trafficked pollutants - and their effects remain for a long period of time. These toxic elements eventually influence the human lives leading to the negative effects on human population growth and its expanding ecological footprint. Even though living organisms have long been subject to a myriad of evolutionary pressures arising from the environment and are consequently well adapted to respond to pressures, the current pace of environmental change is unprecedented and it is unknown whether the capacity of species to adapt to such changes and counteract their harmful and often combined effects may be exceeded. Information and data from reliable sources on this subject is extremely limited, making it difficult to understand the full extent of the effects of environmental change on wildlife health. Recent ecological studies have shown that oxidative status could have a significant impact on fitness components in wild animals, which can predict their chances of reproduction and survival in their natural habitat. Such important characteristics make markers of oxidative status informative tools to evaluate a priority of the individual perspectives of reproduction and survival as well as to assess the effect of human activities on the fitness of species of conservation concern and wildlife in general. Generally stress proteins are activated very early in the cascade of cellular events that follow toxic exposure and at concentrations below the lethal dose. The aim for using stress proteins as preferable biomarkers in environmental risk assessment is to prove that they can give initial information on the effects of pollutants in the shortest period of time. An attempt is being made to review and raise awareness of the conservation practitioners to use these markers of oxidative status to contribute to the success or the failure of reintroduction or translocation programmes; encourage conservation physiologists to enhance the success of conservation of wildlife and its management. This would also address the levels at which anthropogenic environmental change might affect wildlife health and identify potential deficits in reproductive parameters in the context of a rapidly changing environment.

Biography:

Tobias I Ndubuisi Ezejiofor obtained a BSc degree in Medical Laboratory Sciences (Rivers State University of Science & Technology, Port Harcourt), MSc Applied Biochemistry (Nnamdi Azikiwe University, Awka), and PhD Environmental Health Biology (Federal University of Technology, Owerri(FUTO), Nigeria. He is licensed by Environmental Health Officers Registration and Medical Laboratory Science Councils of Nigeria. A member of many professional associations and learned societies, he is a Fellow of the College of Biomedical Engineering and Technology (FCBET), Nigeria. He is a senior Lecturer and heads the Occupational and Environmental Toxicology Research laboratory of the Department of Biotechnology, FUTO, Nigeria. He has published over 25 papers in reputed journals, and serving as reviewer to many such international journals. He had given several conference papers locally and internationally.

Abstract:

Exposures in chemically hostile environments often result in generation of oxidative stress within the body, on account of excessive production of free radicals. The success of the body in dousing the cascade of ill-events associated with the presence of free radicals depends on the availability of equally potent agents that provide counteractive effects to the activities of free radicals. These agents also known as antioxidants give protection to the body by successfully mopping up excess free radicals in the body. Excess of the radicals over that of the body’s antioxidants reserve, as may happen following exposure to toxic organic pollutants in an industrial environment, often favours the establishment of sundry health effects. This study was designed to examine the status of oxidative stress parameters as possible markers of exposure to toxic organic pollutants among petroleum distribution industry workers in Nigeria. Blood sample (5 ml) was collected from each of the 50 study participants consisting of 35 oil workers (exposed), and 15 non oil workers (referents). Standard assay methods were adopted for analyses of the parameters of interest. Result of the study showed that for oil workers, Malondialdehyde (MDA),37.9-96.70 (59.31±11.90 mg/dl), Vitamin C, 0.35-1.52 (0.78±0.28 mg/dl), Vitamin E, 0.22-0.51(0.31±0.06mg/dl), Reduced glutathione (GSH) ranged 0.2-0.8 with a mean of 0.49±0.20 mg/dl; while among the non-oil workers the values were as follows: MDA, 30.3-60.7(49.58±8.12 mg/dl), Vitamin C, 0.41-2.22 (1.26±0.42 mg/dl), Vitamin E, 0.24-1.99(0.44±0.43 mg/dl), GSH, 0.4-1.7 (mean= 0.83±0.32 mg/dl) respectively. A review of the results show that, among the oil workers, the lipid peroxidation substance, MDA was significantly higher (P=0.006) while the antioxidant parameters were significantly lower (p<0.0001), whereas the reverse was the case among the non-oil workers, because MDA was significantly lower in them (P<0.001) even as most of the antioxidant parameters were significantly higher in them. Higher lipid peroxidation substance (MDA) and a dwindling antioxidants status as found among the oil workers gives a clear signal of a higher presence of free radicals that is depleting the antioxidants reserves in the oil workers as compared with the reverse situation among their non-oil work referents, indicating that relative to the referents, the oil workers were most likely to be affected by adverse conditions associated with oxidative stress including a greater tendency to sundry health effects. The results also showed that oxidative stress markers can indeed serve as putative markers of exposure to toxic organic pollutants in the oil and gas industry.

Biography:

Kristen Comfort obtained her PhD in Chemical Engineering from North Carolina State University and completed her Postdoctoral studies as a National Research Council fellow with the Air Force Research Laboratories at Wright Patterson Air Force Base. She is currently an Assistant Professor of Chemical Engineering at the University of Dayton with a joint appointment in Bioengineering. Her research focus is evaluating nanomaterial behavior and subsequent biological responses in enhanced in vitro environments; an area in which she currently has over 10 publications, many of which in high impact journals.

Abstract:

Due to their distinctive physiochemical properties, nanomaterials (NMs) have been incorporated into an increasing number of products and applications. However, studies have identified that these same properties introduce a serious health concern, with NM-dependent toxicity directly correlating to specific physiochemical variables, such as size, composition, and surface coating. While much has been accomplished with regard to basic nanotoxicology, significant alterations to basal biological functionality can occur, even in the absence of cytotoxicity; introducing a novel subset of health concerns. For example, we have shown that chronic exposure to low, sub-toxic dosages of silver NMs produced a long term stress response, genetic modification, and altered cell functionality. Moreover, as NM transport and agglomeration differs from traditional chemicals, due to their insoluble nature, their behavior following cellular exposure is directly relevant to toxicological outcomes. We have identified that multiple in vitro variables, such as fluid composition, dynamic flow, and cellular models modify both NM characteristics and biological responses. A combination of surface chemistry and the composition of the surrounding environment were the critical factors for NM behavior, such as degree of agglomeration and ionic dissolution. The introduction of shear stress through dynamic flow modified the nano-cellular interface through changes to cell morphology and NM deposition efficiency: producing a subsequent shift in the biological response. Therefore, these studies highlight the need for nanotoxicological evaluation to be carried out in a physiologically relevant system in order to best predict potential health concerns associated with NM exposure.

Biography:

Qing Huang has completed his PhD from University of Goettingen in Germany. He is now a Professor in biophysics, the Director of the Department of Physical Biology, Hefei Institute of Physical Science, Chinese Academy of Sciences. He has published more than 80 papers in reputed journals such as J. Am. Chem. Soc., Adv. Mater., Adv. Funt. Mater., Chem. Commun., J. Hazard. Mater., Environ. Sci. Tech., Water Res. and etc. He has served as the reviewers for many international journals, and an expert member for Chinese National Natural Science Foundation.

Abstract:

The increasing industrial use of manufactured nano materials (MNMs) during the last decades poses a potential threat to the environment and in particular to organisms living in the aquatic environment. To evaluate the ecological and human health risks of MNMs released to the environment properly, it is necessary to investigate the involved physicochemical transformations of MNMs under aging process in the environment and their toxicity to hydrophytes such as green algae. In the present study, the physicochemical changes of zinc oxide nanoparticles in aqueous media were characterized by SEM, TEM and XRD, and analyzed quantitatively by means of spectroscopic tools such as Raman and FTIR spectroscopy. The toxicity of zinc oxide nanoparticles under aging process in aqueous media was investigated in green algae Chlorella vulgaris. Our results confirmed the new compounds transformed in aging process which are identified as hydrozincite and zinc hydroxide, and revealed the lower toxicity of aged zinc oxide nanoparticles which is ascribed to the transformations of the aged zinc oxide nano particles. This work has therefore demonstrated the importance of consideration of aging process for evaluation of the toxicity of MNMs in aquatic surroundings.

Biography:

Debjani Nath completed her PhD from Jadavpur University on 1998 and pursued her research endeavor as post doctoral fellow from Indian Institute of Chemical Biology, a premier research institution of India. She has completed her teaching career for fifteen years in University of Kalyani, India and published several papers in international journals of repute and serving as the editorial board member of four international publications.

Abstract:

To develop a toxicokinetic model of acute myelolytic leukemia, benzene was used as a potent leukemogenic agent. The dose, period and time of cumulative benzene exposure of Swiss Albino mice were optimized and survival rate; alteration in cell cycle regulation and other clinical manifestations were analyzed at a cumulative dose of 300ppm × 6 hr. /day × 5 days/week for 2 weeks, i.e., 9000(a) ppm. Analyzing physiological parameters like plasma enzyme profile, complete hematology (Hb %, RBC indices and WBC differentials), hematopoietic cells morphology, expression of cell cycle regulatory proteins, tissue histology and analysis of DNA fragmentation, optimum conditions were established. Elevated level of Plasma AST/ALT with corresponding changes in liver histology of optimally exposed animals also confirmed the toxicokinetic relation of benzne with leukemia. Down regulation of p53 and p21 and up regulation of CDK2, CDK4, CDK6, cyclin D1 and E in this exposed group were marked as the optimum conditions of cellular deregulation for the development of secondary AML. The efficacy of this in vivo model has been tested for chemopreventive activity of two natural phytochemicals like catechin. a natural phenol and antioxidant from Saraca asoca (Roxb.) and monotarpenes from Ocimum basilicum L comparing with known chemotherapeutic drug doxorubicin. It has been concluded that this toxicokinetic model can be utilized as a testing template for the development of multiactive drugs for cancer chemoprevention in the near future.

Biography:

Friday E Uboh completed his Ph.D at the age of 35 from University of Calabar, Calabar, Nigeria, and is presently an Associate Professor of Biochemistry, with Toxicology as his area of research interest. He served as the acting Head of Biochemistry Department in the Department of Biochemistry University of Calabar, Calabar, Nigeria, from 2011 to 2013. Dr. Uboh is a member of Nigerian Society of Biochemistry and Molecular Biology, and Institute of Public Analysts of Nigeria. He has more than 60 papers published in reputable Journals, and is a reviewer and editorial board member of many Journals of repute. He has also presented many conference papers, locally and internationally.

Abstract:

This study assessed the comparative protective potential of vitamins C (vit C) and E against nitrocellulose thinner-induced atherogenicity in male and female albino Wistar rats. Forty eight rats (24 males and 24 females), weighing 180–200 g, were used in the study. The animals were distributed into four groups, with six rats respectively for each of the male and female groups. The animals were orally exposed to 30 mg/kg bwt of nitrocellulose thinner (NCT) and respectively treated with vit C (200.0 mg/kg bwt) and E (100.0IU/kg bwt) daily for 30 days. At end of the experimental treatments, the animals were sacrificed and plasma collected for atherogenicity analyses. The atherogenicity was determined from the plasma total cholesterol, triacylglycerol, low density lipoprotein, high density lipoproteins, and atherogenic indices of the plasma. The atherogenic indices were derived from the plasma lipid ratios, including TC:HDL, TG:HDL, (TC–HDL)/HDL and Log(TC/HDL). The results showed that the levels of plasma TC, TG, LDL, and the atherogenic indices recorded for male and female rats exposed to NCT were significantly (p<0.05) higher, while HDL levels were significantly (p<0.05) lower, compared respectively to the levels recorded for rats in the respective control groups. Also, the increase in TC, TG, (TC–HDL)/HDL and Log(TC/HDL) and decrease in HDL levels reported for rats exposed to NCT were observed to be sex-dependent, with females being more vulnerable. These results also showed that concomitant treatment of the respective groups of rats exposed to NCT with vitamins C and E significantly (p<0.05) protected both the male and female rats against NCT-induced in atherogenicity. However, the protection potential of vitamin E was observed to be significantly (p<0.05) higher than that of vitamin C. The results of this study therefore indicated that oral exposure to NCT may cause a higher risk of atherogenic disorders in females than males; and that vitamin E is more potent than vitamin C in protecting the exposed animals against NCT-induced atherogenicity in male and female rats.

Biography:

Saviour UFOT completed his BSc in Biochemistry and MSc in Pharmacology from University of Calabar and Ibadan respectively. He completed his PhD in Biochemistry (Biochemical and Environmental Toxicology) from University of Calabar in 2014. He was a lecturer in the Department of Pharmacology, University of Ilorin, Nigeria from 1993 to 1998. He is presently working with Total Exploration and Production Nigeria Limited as a Health, Safety and Environment specialist. He has published over 14 papers in reputable journals and has attended many scientific seminars and conferences.

Abstract:

The types and concentration of hydrocarbons accumulated in the serum and liver tissues of male rats orally exposed to bonny light crude oil (BLCO) was assessed in this study. Twenty male albino Wistar rats (180–200 g) used in this study were distributed into two groups (control and test groups), with ten rats each. The test animals were orally exposed to 60 mg/kg bwt of BLCO, once daily for twenty eight days, while the control animals were given distilled water. Twenty-four hours after the last exposure, the animals in both groups were sacrificed under chloroform anesthesia, blood and liver tissues collected for analyses. The whole blood samples were collected by cardiac puncture, allowed to clot, and serum separated after centrifugation. The serum and digested liver tissue samples were extracted and analyzed for hydrocarbon levels using HPLC technique. The results showed that benzene, toluene, ethylmethylene, xylene, BTEX, pyrene, naphthalene and total polycyclic aromatic hydrocarbons (PAH) in the serum (0.066±0.004, 0.641±0.032, 0.470±0.030, 0.112±0.009, 0.370±0.080, 3.660±0.210, 0.009±0.001 12.540±0.720ug/dl, respectively) and liver tissues (0.063±0.003, 0.604±0.024, 0.450±0.034, 0.112±0.009, 0.365±0.080, 3.620±0.190, 0.008±0.002 and 12.680±0.630 ug/g tissue, respectively) of rats exposed to BLCO were significantly (p<0.05) higher, compared to respectively with the concentrations in the serum (0.020±0.001, 0.015±0.001, 0.010±0.000, 0.031±0.001, 0.010±0.000, 1.040±0.010, 0.003±0.005 and 2.270±0.120 ug/dl, respectively) and liver tissues (0.020±0.003, 0.015±0.001, 0.012±0.002, 0.031±0.001, 0.013±0.002, 1.040±0.010, 0.002±0.001 and 2.250±0.120 ug/g tissue, respectively) of control rats. The results of this study indicated that oral exposure to BLCO may results in the accumulation of different hydrocarbons in the blood and liver tissues of rats.

Biography:

K S Tilak is a Doctorate from Andhra University, Waltair, AP, India, the former Dean of faculty of Natural Sciences, Chairman Board of Studies (PG) Zoology and Head of the Department of Zoology and Aquaculture having 40 years of research experience in the field of “Aquatic Toxicology”, having guided 29 research degrees, published 72 research papers in international and national journals recipient of prestigious ‘Archana Gold Medal’ by Academy of Environmental Biology, editor and reviewer of reputed journals, attended and conducted international and national conference in Acharya Nagarjuna University, India.

Abstract:

With the standard methods and guidelines prescribed by EPA for TLC and GLC procedures, the tissues of fish and frog viz. Gill, Muscle, Liver kidney, Brain and Tests (Frog only) were extracted, cleaned up and concentrated to less than one ml and are qualified and quantified. The qualified residues are classified by their standard ‘Rf values’ and are repository at nano level. The residues are varied in different tissues of fish and also in different fish as well as in frog due to lipophillic nature. The latent residues are known to bioaccumulate via the food chain and reach human beings and the risk to the health of the people may be cautioned. The bio-concentrations will show an impact on reproductive impairment of the commercially important fishes and to higher carnivores especially to birds. The need to protect the fast declining population like frogs which are natural pest controllers from under exposure to insecticides cannot be ignored too a part from consumption of fish and frog. In disease management of aqua farming, the chemical treatment is contemplated and use of organo phosphates like chloropyriphos result to reach a level either acute or chronic and the fish are subjected to more stress, avoid feeding which is determintal for their growth. An attempt has been made to study the effect of three mixed pesiticides in ratios as 1:1:1 (Organochlorine-Endosulphate, Organophosphate-Dimetheote and a Synthetic pyrathrod Cypermethrin. The results of the study revealed that prolonged exposure to sublethal concentration of mixture of pesticides ratios in the fish Labeo rohita leads to increased accumulation. The study also revealed that at sublethal concentrations of pesticide mixture lead to high residue concentrations. The uptake and persistence of endosulphan, dimetheote and cypermethrin varies according to the residues which is a prerequisite to observe any biochemical or histopathological change which are really the indices of toxicity. It is also confirmed that many of the bio chemical changes in the tissues works from their normal functions and triggers a cascade mechanism that reverberate.