Biography:

Ping Song has completed his PhD in 1994 from Texa Tech University. He is a global regulatory team leader for seeds/traits in Dow Agro Sciences LLC, a R&D driven agricultural company. He has published two book chapters and more than 25 papers in peer-reviewed journals.

Abstract:

When evaluating the potential cross reactivity of a novel protein with known allergens, amino acid sequences are often compared using bioinformatic approaches. A high quality curated database containing allergen sequences is a fundamental requirement for executing sequence comparisons. Existing sequence comparisons have been based on sequence similarity, identical short-mer amino acid matches, motif identification, machine-learning models, and 3-D structure prediction. Tools based on these approaches are publically available and have been investigated for their sensitivity and selectivity. Although fraught with poor specificity and other technical issues, the FAO/WHO/Codex Alimentarius method is the standard for regulatory submissions to government agencies. This approach involves searching for >35% identity over 80 amino acids or more by local alignment algorithms such as FASTA or BLAST. However, the literature has clearly demonstrated that use of amino acid similarity in combination with a statistical measure of power, like E-values, can be equally sensitive but with greater specificity (fewer false-positives). A one-to-one FASA comparison with a biologically relevant E-value as a criterion is such an approach, and this method additionally avoids some of the technical shortfalls of an amino acid identity-based algorithm. In the future, modern genome sequencing techniques offer the promise of increasingly powerful bioinformatic analysis of food proteins for allergenic risk.

Biography:

Amr Amin has completed his PhD at University of Illinois at Chicago and received a Post-doctoral training in the field of molecular genetics at University of Pennsylvania School of Medicine. He started his academic career at UAE University where he currently serves as a Full Professor of Cell Biology. His research focuses on ways to control cancer, particularly liver cancer. He has published many research articles and reviews and serves as reviewer and as an editorial member of many specialized peer-reviewed journals. He is also a member of many specialized societies and the sole recipient of multiple national and international scientific awards.

Abstract:

Liver cancer is the second most common cause of cancer-related death worldwide. The prognosis of patients with liver cancer is usually poor; hence, a novel approach against liver cancer is essential for a better therapeutic outcome. Saffron and its active constituents were reported to have antioxidant, anti-inflammatory and anti-tumor properties. The aim of this study was to investigate chemopreventive action of crocin, one of the promising active constituents of saffron, against diethylnitrosamine (DEN)-induced liver cancer in rats, and the possible mechanisms by which crocin exerts its anti-tumor effects. Findings reported herein demonstrated the anti-proliferative and pro-apoptotic properties of crocin when administrated in DEN-treated rats. Additionally, crocin exhibited anti-inflammatory properties that inhibited NF-kB, among other inflammatory markers. According to our network analysis, NF-kB was identified as a regulatory hub and therefore, a candidate therapeutic drug target. Together, these findings nominate crocin as a candidate chemopreventive and therapeutic agent against HCC.

Biography:

Dr. Sakhila Banu obtained her Bachelors and Master’s degrees from the Madurai Kamaraj University, India. She completed her MPhil and PhD degrees in Endocrinology from the University of Madras, India and pursued her post-doctoral fellowships at the Laval University and University of Montreal. She is currently an Assistant Professor in the Department of Veterinary Integrative Biosciences (VIBS), College of Veterinary Medicine & Biomedical Sciences, Texas A&M University. She started an effective interdisciplinary research program in the field of female reproductive toxicology. Her major goal is to understand the adverse effects of chromium VI, a heavy metal endocrine disruptor in the environment, on female fertility and fetal development. Her research has been funded by the National Institute of Environmental Health Sciences (NIEHS) and the Department of Defense, and other private foundations. She received several awards such as USDA-NRI Merit Award, and Outstanding Scientific Achievement Award, College of Veterinary Medicine & Biomedical Sciences. Her specific research goal is to develop a strong basic research program in Reproductive Toxicology that can be translated to identify new intervention strategies for mitigating adverse effects of heavy metal endocrine disrupting chemicals (EDCs). Her long-term goals are two-fold: 1) to understand the molecular mechanism of heavy metal-induced adverse effects on ovarian and uterine function, pregnancy outcome, and placental and fetal development; 2) to understand the protective effects of various natural and synthetic antioxidants (such as edaravone, glutathione, vitamin C and resveratrol) against the deleterious effects of heavy-metal EDCs.  Current research in her lab is focused on the study of reproductive and developmental toxicity of hexavalent chromium (CrVI). Drinking water contamination with CrVI in the United States is a growing problem due to increased usage of CrVI and improper disposal of Cr waste into the environment. Significant contamination with CrVI has been found in the drinking water sources of all the states in the U.S. Effects of Cr on reproductive health in women and development in children have received less attention. Epidemiological data document that women exposed to Cr in environmental or occupational settings suffer from infertility, gynecological problems, congenital malformation of fetuses, neonatal mortality, and premature abortions with increased levels of Cr in their blood, urine and placenta. Cr can bind directly to DNA and nuclear proteins, cause DNA strand breaks and mutations, alter the balance between reactive oxygen species (ROS) and antioxidants, and activate several cell signaling pathways. Therefore, her current research objective is to determine molecular pathways and identify target genes/proteins by which Cr alters prenatal development and organogenesis of female reproductive system in the offspring.

Abstract:

Environmental exposure to endocrine disruptors (EDCs) is linked to several ovarian diseases such as premature ovarian failure, polycystic ovary syndrome, early menopause and infertility in women. Hexavalent chromium (CrVI) is a heavy metal EDC, widely used in more than 50 industries including chrome plating, welding, wood processing and tanneries. Recent data from USEPA indicate increased levels of Cr in drinking water from several cities in the US, which predisposes Americans to various health problems. Our previous findings demonstrated that prenatal and early postnatal exposure to CrVI caused ovarian failures in F1 offspring. Two main goals of our laboratory are to identify the molecular mechanism behind CrVI-induced reproductive failure, and to identify intervention strategies to mitigate CrVI-induced female reproductive failures. Pregnant rats were treated with potassium dichromate (CrVI) during prenatal period (gestational days) 9.5-14.5, or postnatal period from postnatal day (PND)-1 - 21, through drinking water, and the fetuses or pups were exposed to CrVI through transplacental transfer and mother’s milk, respectively. Ovaries were removed from the fetuses and postnatal rats, and various analyses were performed. Results showed that gestational exposure to CrVI: (i) increased germ cell/oocyte apoptosis and advanced germ cell nest (GCN) breakdown; (ii) increased POF markers spatio-temporally during GCN breakdown; and (iii) decreased POF markers during postnatal follicle development. Resveratrol (RVT), a polyphenolic component in grapes and red wine, has been known for its cytoprotective actions against several diseases. However, beneficial effects of RVT against early exposure to endocrine disrupting chemicals (EDCs) has not been understood. Lactating mother rats that were exposed to CrVI received resveratrol (RVT) supplementation (10 mg/kg body wt., through oral gavage daily). Lactational exposure to CrVI increased atresia of follicles by interfering with steroidogenic pathway and oxidative stress pathways. RVT mitigated the effects of CrVI and protected against CrVI-toxicity of the ovary.

Biography:

Bethany R Baumgart completed her Bachelor of Science degree in Biology in 2009 and Master of Science degree in Biology and Biotechnology in 2011, both from Ball State University. She is a Research Scientist I in Toxicology at Bristol-Myers Squibb Company with roles as a member of the Molecular and In Vitro Toxicology Laboratory as well as nonclinical study director.

Abstract:

Pharmaceutical formulations (vehicles) used to administer test articles to animals often contain excipients to enhance delivery of the test compound. The common excipient d-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) increases solubility and maximizes systemic exposure of lipophilic test articles. Given the well established antioxidant properties of d-α-tocopheryl succinate (TS), a component of TPGS, and d-α-tocopherol (TOC), hydrolyzed TS, we examined the potential protective effects of vehicles containing TPGS. Such effects could mask potential toxicities of test articles, including processes involved in carcinogenesis, and impact nonclinical safety assessments. Male and female Sprague-Dawley rats were administered vehicles containing 5% or 40% TPGS (70 or 550 mg/kg/day TS, respectively) orally for 1 week. A control group was administered polyethylene glycol-400 (PEG-400; no vitamin E) orally and positive control animals received a single 100 mg/kg intraperitoneal (IP) injection of TS. Additionally, whole blood from untreated animals was incubated with 5 or 50mM H₂O₂ ex vivo with or without TS (0.5, 5, 50, or 500μM) or ascorbate (1mM), as a positive control, for 1 hour. Plasma, liver, and adrenal gland concentrations of TS and TOC as well as oxidative status of plasma were evaluated following oral administration of TPGS-containing vehicles, IP injection of TS, or treatment of whole blood with H₂O₂ ex vivo. Oral TPGS administration did not affect TOC concentrations in plasma or adrenal glands and caused only transient increases in liver. Concentrations of TS in plasma, liver, and adrenal glands were undetectable in control animals, but increased with administration of vehicles containing 5 and 40% TPGS. Oral administration of TPGS did not reduce plasma lipid peroxidation in vivo. Substantially greater TS concentrations (100× greater than in vivo) added to H₂O₂-treated whole blood ex vivo were also unable to reduce lipid peroxidation. These results provide evidence that administration of oral TPGS vehicles is unlikely to impact nonclinical carcinogenicity safety assessments of pharmaceuticals.

Biography:

Grace-Anne Bent has received PhD from University of the West Indies. She is a lecturer of analytical chemistry in the Department of Chemistry at The University of the West Indies, St. Augustine Campus, Trinidad and Tobago. Her research interests include food safety and security, investigating the chemistry of food and food related toxins in an effort to minimize human exposure by understanding their mechanisms of interaction (in vivo and in vitro). She has published a book and 7 journal articles. She is also the recipient of several research awards.

Abstract:

Exposure to acrylamide (AA) or its metabolite glycidamide (GA), in foodstuffs, is a major concern today. This paper communicates recent developments concerning the role that AA and its metabolite GA, potentially toxic food contaminants, produced on frying, steaming (heat treatments above 100^oC) carbohydrate-based foodstuff via Maillard reaction involving asparagine and reducing sugars. It has been proposed that detoxification of AA and GA occurs primarily via conjugation with thiols via the Michael-addition reaction. Recent investigations to study the reactivity of thiols towards AA and GA included the use of: glutathione (GSH), L-cysteine (CySH) and captopril (CapSH). GSH and CySH are naturally occurring in the body while CapSH is synthetic and usually administered in the form of a drug used for the treatment of congestive heart failure. The kinetic rates of conjugation reactions follow: CySH>GSH>CapSH as opposed to CySH>CapSH>GSH expected based on molecular sizes. Preliminary comparative DFT (density functional theory) calculations on AA and thiols provide information that close hydrogen interactions between GSH and AA; which is absent in CySH and CapSH explains the observed rate trend. Furthermore, preliminary DFT calculations show that there is an open question of H-transfer via intra-molecular GSH or H-transfer via solvent water molecules.

Biography:

Margarita C. Curras-Collazo completed her Ph.D in Medical Physiology from The Ohio State University and postdoctoral studies in neuropharmacology at the University of North Carolina, Chapel Hill and at Emory University. She is an Associate Professor of Neuroscience in the Department of Cell Biology & Neuroscience at the University of California, Riverside. Research in the Curras-Collazo lab focuses on transcellular and biochemical mechanisms underlying neurosecretion in the neuroendocrine hypothalamus as well as the neurotoxicological and endocrine disruptive effects of environmental pollutants such as brominated flame retardants. She has published more than 35 papers in reputed journals and has served as an ad hoc reviewer for the National Science Foundation, American Heart Association, and Department of Defense as well as international agencies.

Abstract:

Organohalogen pollutants such as polychlorinated biphenyls (PCBs ) and polybrominated diphenyl ethers (PBDEs) act as endocrine disrupting chemicals. We have also shown that these toxicants alter vasopressin neurosecretion from magnocellular neuroendocrine cells of the supraoptic nucleus of the rat hypothalamus (SON) and osmoregulatory capacity mediated by vasopressin.  Because VP responses to hyperosmotic stimulation are regulated by nitric oxide (NO) signaling, we studied NO synthase (NOS) activity in the SON as potential target of PCB-induced disruption of neuroendocrine processes. To examine PCB-induced changes in NOS activity under normosmotic and hyperosmotic conditions, male Sprague-Dawley rats were exposed to the industrial PCB mixture, Aroclor 1254 (30 mg/kg/day) during gestation.  NADPH-diaphorase (NADPH-d) activity assessed in SON sections at 3 ages: postnatal day 10, early adult (3-5 months) or late adult (14-16 months). Hyperosmotic treatment increased mean NADPH-d staining density of oil hyperosmotic controls by 19.9% in early adults and 58% in late adulthood vs normosmotic controls. In utero exposure to PCBs occluded hyperosmotic-induced upregulation of NADPH-d activity to control levels in early adults. In contrast, rats that received PCB exposure as early adults orally for 14 days displayed normal NOS responses to hyperosmotic stimulation. Therefore, our findings show that developmental but not adult exposure to PCBs significantly reduces NOS responses to hyperosmolality in neuroendocrine cells. Late adulthood hyperosmotic rats still displayed 28% reduced NOS activity and reduced osmoregulatory capacity during osmotically activated conditions produced by in utero exposure. Plasma osmolality values were 375.0 ± 9 vs 348.6 ± 8 mOsm/L for hyperosmotic late adult rats treated with A1254 vs oil controls, respectively. These findings suggest that developmental PCBs permanently compromise NOS signaling necessary for activated neuroendocrine responses with potential osmoregulatory consequences.

Biography:

Alexei Basnakian received his PhD and DSc degrees from the Russian Academy of Medical Science, both in the field of DNA endonucleases. He had postdoctoral trainings in molecular biology at the Harvard Medical School and in toxicology/cancer research at the National Center for Toxicological Research. Dr. Basnakian is Professor in the Department of Pharmacology and Toxicology, and Director of the DNA Damage and Toxicology Core Center at the University of Arkansas for Medical Sciences, and Research Career Scientist at the Veteran’s Hospital in Little Rock, Arkansas, USA. He is an author of more than 85 peer-reviewed papers and 12 reviews or book chapters. Dr. Basnakian is an Editorial Board member of several biomedical journals, and a member of NIH and VA grant study sections. His research interests are in DNA endonucleases and DNA damage associated with toxicity, anti-cancer therapy, cell injury and cell death.

Abstract:

Apoptotic endonucleases are the enzymes that universally induce irreversible cell death by fragmenting DNA in response to cell injury. While most of the DNase/endonuclease activity is used after cell death, the latest studies showed that genetic inactivation of some endonucleases provide protection of cells and tissues against DNA breaks induced by cytotoxic stimuli. These data suggest that DNases act before the “point of no return” in cell death, and display a possibility for new therapeutics aimed to inhibit endonucleases for tissue protection. However, inhibitors of apoptotic endonucleases are not available. We have developed several high throughput screening assays based on a proprietary fluorescent probe. This assays applied in solution allowed the identification of several new inhibitors of two apoptotic DNases, deoxyribonuclease I (DNase I) and endonucleases G (EndoG). The DNase inhibitors were able to partially protect kidney cells and mice from cisplatin toxicity. These or similar assays have a great promise as tools for new drug discovery.

Biography:

Dr. Renee S Arias in 1988-1992 was Quality control of inoculants based on symbiotic nitrogen fixing bacteria (Rhizobium spp. and Bradyrhizobium japonicum), and effect of fungicides on pre-inoculated leguminous seeds for Rhizobacter Argentina Co., Argentina. He was Teaching Assistant Plant Microbial Interactions, two semesters, Department of Plant Pathology, University of Hawaii, Spring 1995 and Spring 1997. From 2000 – 2002 he was Research Associate, HARC (Hawaiian Agriculture Research Center).  2011 to present Dr. Renee S Arias is a Research Pathologist, at the USDA-ARS-SAA, Peanut diseases with focus on Aflatoxin.

Abstract:

Approximately 4.5 billion people are chronically exposed to aflatoxins, these are powerful carcinogens produced by Aspergillus flavus and A. parasiticus.  High levels of aflatoxins in crops result in approximately 100 million metric tons of cereals, nuts, root crops and other agricultural products being destroyed or diverted to non-human consumption each year.  We have targeted silencing of 5-genes in the aflatoxin biosynthesis pathway of Aspergillus by RNA interference (RNAi) from the plant host to reduce/eliminate aflatoxin accumulation in peanut and maize seeds.  Given that no method existed to analyze the effectiveness of RNAi against aflatoxins, and that testing of hundreds of plants in the field under aflatoxin-conducive conditions is not an option in this case, we developed a method of challenging with aflatoxigenic Aspergillus the RNAi treated seeds, and then analyze those seeds by ultra-performance liquid chromatography (UPLC). In parallel, we developed a workflow to obtain information of those isolates at the DNA sequencing level. This workflow includes fungal isolation, 25 InDel fingerprinting followed by cluster analysis, and whole genome sequencing of clade representatives. This method also allows analysis of small seed pieces for gene expression by real-time PCR (RT-PCR) and small RNA sequencing.  Solving the aflatoxin problem in crops would be equivalent to increasing food production by millions of tons that could be safely consumed instead of being discarded or diverted to other uses.

Biography:

Lawrence C Sowers received his PhD in Physical Biochemistry from Duke University. Following Post-doctoral positions at Harvard and the University of Southern California, he began his independent career at the City of Hope National Medical Center. He then moved on to Loma Linda Medical School and then to the University of Texas Medical Branch where he is currently Professor and Chair of the Department of Pharmacology and Toxicology. He is currently a member of the Cancer Etiology study section and a Member of the Editorial Board of the Journal of Biological Chemistry.

Abstract:

The DNA of all organisms undergoes persistent DNA damage and repair. Additionally, DNA bases undergo enzymatically-mediated modifications involved in both stem cell differentiation and increased immune diversity. Many of these modified bases are removed from DNA by glycosylases of the base excision repair system. Therefore, the released free bases represent the end product of DNA metabolism in most organisms. While a substantial number of investigations have focused on the identification and measurement of modified bases in DNA, few have examined the free bases products released either spontaneously or enzymatically. We have developed a method for examining free bases in extracts of animal tissues which involves HPLC separation followed by GC/MC/MS analysis using stable isotope analogs. The challenges and advantages of this method, which has been applied to the normal rodent brain, will be discussed.

Biography:

Abstract:

The replication-dependent histone genes are the only metazoan genes whose messenger RNA (mRNA) does not terminate with a poly(A) tail at the 3’ end. Instead, the histone mRNAs display a stem-loop structure at their 3’ end. Stem-loop binding protein (SLBP) binds the stem-loop and regulates canonical histone mRNA metabolism.   We report that exposure to arsenic, a carcinogenic metal, decreases cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms. Notably, arsenic exposure dramatically increases polyadenylation of canonical histone H3.1 mRNA possibly through downregulation of SLBP expression. The polyadenylated H3.1 mRNA induced by arsenic is not susceptible to normal degradation that occurs at the end of S phase, resulting in continued presence into mitosis, increased total H3.1 mRNA, and increased H3 protein levels.  Excess expression of canonical histones has been shown to increase sensitivity to DNA damage, as well as increase the frequency of missing chromosomes and induce genomic instability. Our hypothesis is that H3.1 genes are initially transcribed with a normal stem-loop construct at the 3’ end of the mRNA. Arsenic depletes nuclear levels of SLBP resulting in H3.1 transcripts unbound to SLBP. These unbound transcripts lose their stem-loop structure at the 3’ end and acquire a poly(A) tail, which increases the half-life and facilitates translation of the mRNA, two factors that provide for increased H3.1 protein levels.  The poly(A) H3.1 mRNA is not susceptible to normal degradation that occurs at the end of S phase allowing for its presence in other phases of the cell cycle. Over-expression of SLBP suppressed the effect of As on H3.1 polyadenylation.   Knockdown of SLBP by siRNA induced anchorage independent growth of BEAS2B cells.  Transfection of Polyadenlated H3.1 but not H3.3 also induced anchorage independent growth in BEAS2B cells. Anchorage independent growth was also induced in human Urothelial cells by transfection of polyadenylated H3.1 but not H3.3.

Biography:

Amira Amin Wahdan has completed her Doctorate degree from Tanta University. She is a lecturer in Forensic Medicine and Clinical Toxicology department, Faculty of Medicine, Tanta University. She is a reviewer in reputed journal.

Abstract:

Metal phosphides are highly effective insecticides and rodenticide. They are used as a cheap rodenticide in developing countries. The aim of this study was to detect the incidence of methemoglobinemia and intravascular hemolysis in some cases of acute phosphide poisoning. This is a cross sectional study which was conducted on 50 cases suffering from acute metal phosphide poisoning admitted to Tanta toxicology unit, from October 2014 till March 2015. For each case, the following were done: history taking, physical examination and laboratory investigations (including measurement of methemoglobin (Met-Hb) level, arterial blood gas analysis, routine investigations, lactate dehydrogenase enzyme and complete blood picture with reticulocytic count). Eight cases (16%) had combined methemoglobinemia and hemolysis. Aluminum phosphide was the toxic agent in seven of them and zinc phosphide in only one. Three cases (6%) had methemoglobinemia alone; one of them was poisoned by aluminum phosphide and the other two by zinc phospide. Another three cases had hemolysis alone; one of them was due to aluminum phosphide and the other two were due to zinc phospide. So the present study included a total of eleven cases (22%) of methemoglobinemia. The mean Met-Hb level was 14.45±9.32% and1.63±0.45% in cases with high and normal Met-Hb level respectively, with a significant statistical difference between both. Furthermore, the mean oxygen saturation showed a significant statistical difference between both. A total of eleven cases (22%) of hemolysis were also included. It was concluded that methemoglobinemia and hemolysis can complicate the course of acute phosphide poisoning.

Biography:

Natasa Petronijevic, MD, PhD has finished her PhD thesis in 2001 at the School of Medicine, University of Belgrade, Serbia. She is a specialist of Clinical Biochemistry and Laboratory Medicine. She is a project leader of scientific projects financed by Serbian Government Ministry of Science and a reviewer in several respectable international journals. She is a course Director of Medical Biochemistry and Director of PhD studies of Neuroscience at the School of Medicine, University of Belgrade. She is a President of Section for Clinical biochemistry, Serbian Medical Society. She has published more than 35 papers in reputed journals.

Abstract:

Association of aluminum (Al) and some neurodegenerative disorders, including Alzheimer’s disease (AD), is implicated in 1965 when Al was recognized as neurotoxin. Since then, the role of Al as a pathogenetic factor in AD was suggested by many epidemiological studies. The exact mechanism responsible for changes induced by Al is not known. We have analyzed the effects of ingested Al on the acetylcholinesterase (AChE), NADPH oxidase (NOX2), respiratory chain enzymes and oxidative stress parameters in Mongolian gerbils brain. Also, the protective effects of intrahippocampal application of green tea leaf extract and glucose-6-phosphate dehydrogenase on aluminium-induced brain toxicity were studied. Adult gerbils were acutely (LD₂₅), or subacutely (LD₁₀) exposed to aluminum chloride by gavage and sacrificed 2, 6 or 24 hours after acute and 21 days after sub-acute treatment. Intrahipocampally solutions were injected into the CA1 region using a stereotaxic frame for small animals. The expressions of amyloid and tau protein, as well as, membrane-bound (gp91phox, p22phox) and cytosolic (p40phox, p47phox, p67phox) NOX2 subunits, the activity of AChE and oxidative stress parameters were determined in specific brain structures. Changes of AChE and COX activities, as well as, oxidative stress parameters were seen as the earliest effects of Al treatment. The changes of the expression of NOX subunits were seen six hour after acute poisoning. After subacute Al ingestion the oxidative stress was pronounced. Decreased gp91phox and increased p67phox expressions were seen in cortex while in the hippocampus the decrease of p67phox was noticed. Green tea leaf extract and glucose-6-phosphate dehydrogenase have shown protective effects.

Biography:

Swati Omanwar completed her PhD in 2008 in Medical Physiology from Faculty of Medical Sciences, University of Delhi. She is presently as Scientist at School of Sciences, Indira Gandhi National Open University, New Delhi. She has published more than 17 papers in reputed journals and has been serving as reviewer for many.

Abstract:

Mercury, a heavy metal belonging to the transition element series of the periodic table, is widespread and persistent in the environment as an industrial pollutant. Any pollutant affecting human is transported to various organs by the cardiovascular system. Epidemiological and animal studies have suggested a strong association between the environmental and occupational exposure to mercury and risk of cardiovascular diseases (CVD). Toxicity from mercury is associated with in vivo oxidative stress. Mercury exposure induce the generation of reactive oxygen species (ROS) with subsequent oxidative damage in several organs and systems, as well as alter the antioxidant defence system in cells (6-10).Vascular endothelium, is very sensitive to oxidative stress and plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. Oxidative stress which results in endothelial dysfunction and loss of endothelium dependent vasorelaxation is one of the most commonly observed cardiovascular effects of mercury exposure. The endothelium can evoke relaxations and contractions of the underlying smooth muscle, by releasing vasoactive agents. Nitric oxide (NO), formed by endothelial NO synthase (eNOS), is the best characterized endothelium derived relaxing factor (EDRF). The release of NO is down regulated/upregulated by factors like oxidative stress, estrogen and diseases like diabetes and hypercholelestrolemia etc. The inhibition/activation of eNOS by mercury, affecting the NO release is majorly regulated by superoxide anions and minorly may be by insulin, estrogen, omega 3 unsaturated fatty acid and hypercholesterolemia and is one of the proposed mechanisms for mercury-induced vascular diseases. In addition, during exposure to mercury, overproduction of reactive oxygen species (ROS) can occur, resulting in oxidative stress, which is another major risk factor for endothelial dysfunction.

Conclusion: NO signaling mechanism and oxidative stress play a vital function in the mercury –induced cardiovascular diseases in the populations exposed to mercury.

Biography:

Mercy Ekwere has over 20 years of teaching experience in Biochemistry. She is rounding up her PhD under Associate professor F E Uboh and assisting in the supervision of Dr Uboh’s students. She has several publications to her credit.

Abstract:

Crude oil composition varies slightly by its source but contains many chemicals with toxic properties that are fairly in animals and human. Male and female albino rats weighing between 120kg and 200kg were grouped separately into test groups and control groups. Each group had five rats and was administered 60mg/kg body weight of crude oil orally for 28 days except for the control groups. The total body weights were taken at 7days interval for 28 days. Results showed a progressive decrease in total body weight of rats and a significant (p<0.05) decrease in average body weight of both male and female albino rats compared with respective control groups. Additionally, all test animals exhibited adverse reactions like itching watery eyes, sleepiness, shortening of breath and release of mucous. Also, there was a marked sign of dehydration and impaired digestion in week four of administration.