Day 2 :
- Workshop on Natural Antimutagens
Location: DoubleTree by Hilton Philadelphia Airport
Session Introduction
Marcela Rizzotto
Rosario National University, Argentina
Title: Natural antimutagens
Time : 09:00-09:30
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.
- Track 3: Genetic Toxicology
Location: DoubleTree by Hilton Philadelphia Airport
Chair
Marcelo L. Larramendy
National University of La Plata, Argentina
Co-Chair
Rutao Liu
Shandong University, China
Session Introduction
Michael Fasullo
State University of New York Polytechnic Institute, USA
Title: Determining genetic susceptibility to food carcinogens using Saccharomyces cerevisiae (Budding Yeast)
Time : 09:30-09:50
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).
Silma Regina Ferreira Pereira
Federal University of Maranhão, Brazil
Title: Does antileishmanial glucantime® cause DNA damage by oxidative stress?
Time : 09:50-10:10
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.
Arpiné Ardzivian Elnar
Université de Lorraine, France
Title: Toxicogenomic profiles in neurons of male mice following early low exposure to the six indicator non-dioxin-like polychlorinated biphenyls
Time : 10:10-10:30
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.
Marcela Rizzotto
Rosario National University, Argentina
Title: Chemopreventive action of L-ascorbic acid and green tea infusions on the acute toxicity and mutagenicity of reaction mixtures nitrite-sulfonamide
Time : 10:30-10:50
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.
G Wultsch
Medical University of Vienna, Austria
Title: Use of exfoliated buccal and nasal cells for the detection of acute and genotoxic effects caused by occupational and life-style exposures
Time : 11:10-11:30
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.
Rutao Liu
Shandong University, China
Title: Mechanisms and modes of lead action on SOD inactivation in zebrafish livers
Time : 11:30-11:50
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.
Syamantak Mani Tripathi
Chhattisgarh Kamdhenu Vishwavidyalya, India
Title: Amelioration of sub-chronic acephate induced immunotoxic effects by Achyranthes aspera and Phyllanthus niruri in white leghorn cockerels
Time : 11:50-12:10
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.
K S Tilak
Acharya Nagarjuna University, India
Title: Studies on some biochemical and genotoxic changes of organophosphorus pesticides in agricultural sprayers of Krishna district, A.P. India
Time : 12:10-12:30
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 Toxicologyâ€, 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.
- Track 4: Toxicity Testing Market & Business Opportunities
Track 5: Environmental Toxicology
Track 6: Regulatory Toxicology
Location: DoubleTree by Hilton Philadelphia Airport
Chair
Diana Anderson
University of Bradford, UK
Co-Chair
Alenka Franko
University Medical Centre, Slovenia
Session Introduction
Diana Anderson
University of Bradford, UK
Title: The protective effect of the flavonoids on food-mutagen-induced DNA damage in peripheral blood lymphocytes from colon cancer patients
Time : 13:10-13:30
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.
F Balszuweit
Bundeswehr Institute of Pharmacology and Toxicology, Germany
Title: Co-culture of immortalized keratinocytes and immune cells to investigate sulfur mustard toxicity and potential treatments
Time : 13:30-13:50
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.
Lenita de Freitas Tallarico
State University of Campinas, Brazil
Title: Relevance of assays using mollusks and perspectives in environmental risk assessment
Time : 13:50-14:10
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.
Alenka Franko
University Medical Centre, Slovenia
Title: The gene-environment interactions and asbestosis
Time : 14:10-14:30
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.
Ying Peng
Sun Yat-sen University, China
Title: Autophagy alleviates the memory impairment caused by morphine through inflammation suppression in hippocampi of C57BL/6 mice
Time : 14:30-14:50
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.
F Balszuweit
Bundeswehr Institute of Pharmacology and Toxicology, Germany
Title: Silibinin as a potential therapeutic for sulfur mustard injuries
Time : 14:50-15:10
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.
Shou-Lin Wang
Nanjing Medical University, P. R. China
Title: Environmental exposure to BDE47 is associated with the risk of diabetes: a community-based case-control study and an animal experiment
Time : 15:10-15:30
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.
Heba Youssef
Port Said University, Egypt
Title: Monosodium glutamate-induced cerebellar toxicity: Possible role of nitric oxide in adult albino rats
Time : 15:30-15:50
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.
Olujimi O O
Federal University of Agriculture, Nigeria
Title: Occurrence, removal and health risk assessment of phthalate esters: A case study of two different wastewater treatment processes in Lagos and Ogun State
Time : 15:50-16:10
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.
Poster Presentations 16:10-17:00 @ Foyer
Sharda Shah Peshin
All India Institute of Medical Sciences, India
Title: Tele consultations to the National Poisons Information Centre, AIIMS, New Delhi: A retrospective study
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.
S S Hundal
Punjab Agricultural University, India
Title: Environmental pollution, stress molecules and wildlife health: An overview
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.
Ezejiofor Tobias I Ndubuisi
Federal University of Technology, Nigeria
Title: Oxidative stress parameters as markers of exposure to toxic organic pollutants among petroleum distribution industry workers in Nigeria
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.