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Organochlorine pesticides mixture exposure assessment and DNA damage in mother–child pairs in agricultural community in San Luis Potosi, Mexico
S208
Abstracts / Toxicology Letters 189S (2009) S57–S273
Z02 Organochlorine pesticides mixture exposure assessment and DNA damage in mother–child pairs in agricultural community in San Luis Potosi, Mexico ˜ 1 , Regina Montero 2 Diana Alvarado 1,∗ , Leticia Yánez UASLP, Environmental Toxicology, San Luis Potosi, Mexico, 2 UNAM, Genomic Medicine and Environmental Toxicology, Mexico City, Mexico
1
Fifty mother–child pairs from an agricultural community in San Luis Potosí, Mexico were studied, in order to evaluate exposure to organochlorine pesticides mixtures and genotoxic damage, obtaining from them maternal and umbilical cord blood samples. In order to evaluate organochlorine pesticides exposure, 15 pesticides were quantified by using a gas chromatograph electroncapturing detector, and a mass spectrometry detector in maternal as well as in cord plasma. DNA damage was evaluated by comet and clastogenic damage assay. The organochlorine pesticides concentration range in maternal plasma samples was from 5000 to 25,500 ng/g fat. Comet assay was evaluated using olive tail moment (fluorescence intensity and tail length); considering 4 as the reference value, 60% of the mothers, and 78% of the babies manifested damage. In regard to clastogenic damage, this was reported as micronuclei, chromatin buds and nucleoplasmic bridges frequency in every 1000 cells evaluated. For mothers, a range from 0.33 to 5 was obtained, whereas in newborns it was from 0 to 8. The frequency in a non-exposed population is from 0 to 3. The diffusion capacity through placenta of this kind of pollutants was shown, because plasmatic concentrations in the umbilical cord plasma were detected in a range from 9800 to 285,500 ng/g fat. When analyzing the mother’s DNA damage versus the baby’s DNA damage, a statistical significance was observed, not occurring this in clastogenic damage. 84% of the mothers took a folic acid supplement during their pregnancy; it has been reported that this micronutrient has the property of avoiding or repairing DNA damage, which drives us to the hypothesis that folic acid intake might be a crucial fact to avoid genotoxic damage, even though the developing fetus was exposed to organochlorine pesticides, being these results interesting since this kind of population has not been studied in this regard. doi:10.1016/j.toxlet.2009.06.537
Z03
夽 Effects of methiocarb on lipid peroxidation in rat tissues Sibel Özden ∗ , Buket Alpertunga Faculty of Pharmacy, Department of Toxicology, Istanbul, Turkey Methiocarb (3,5-dimethyl-4-(methylthio)phenol methylcarbamate) is an N-methylcarbamate insecticide used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. The aim of this study was to investigate the possible effects of methiocarb to induce lipid peroxidation in tissues of male Wistar rats following of 1-, 5- and 28-day exposures. Animals were divided into six different groups and methiocarb was administered by orally at doses 25, 10 and 2 mg/kg b.w. for 1-, 5- and 28-day, respectively. Liver, kidney, brain and testis tissues were taken from the rats for the biochemical examinations. Lipid peroxidation and reduced
glutathione (GSH) levels were determined in the tissues. Lipid peroxidation was significantly increased in liver, kidney, brain and testis after 1-, 5- and 28-day treatments of methiocarb. GSH levels were significantly increased in 1-day period and significantly decreased in 5- and 28-day periods in all tissues after methiocarb administration. These findings demonstrated that 1-day high dose and 5- and 28-day lower doses treatments of methiocarb may induce lipid peroxidation and have disturbances in the GSH levels in liver, kidney, brain and testis supporting that free radicals may be involved in the mechanism of methiocarb-induced toxicity. Methiocarb-induced toxicity via lipid peroxidation and free radical mechanism has not been previously reported and therefore, this study represents a possible pathway for the mechanism of methiocarb-induced toxicity. Further investigations are required to better understand the mechanisms of oxidative stress in the toxicity of methiocarb. Keywords: Methiocarb; Lipid peroxidation; Glutathione; Liver; Kidney; Brain; Testis 夽 Selected for Oral Presentation. doi:10.1016/j.toxlet.2009.06.538
Z04 Effects of subchronic terbutryn exposure on some biochemical, haematological and histopathological parameters of the common carp (Cyprinus carpio L.) Josef Velisek ∗ , Eliska Sudova, Jana Machova, Zdenka Svobodova University of South Bohemia Ceske Budejovice, Research Institute of Fish Culture and Hydrobiology, Vodnany, Czech Republic S-triazines constitute a group of similar herbicides used extensively in agriculture and non-agricultural use sites, primarily to control broadleaf and some grassy weeds, that have become ubiquitous contaminants of the environment. Due to their heavy use in agriculture and to their persistence, many of these compounds present in surface and ground waters, and have to be considered a potential risk for water life as well as for drinking water quality. The aim of the study was to evaluate subchronic toxic effects of the terbutryn (N-(1,1-dimethylethyl)-N -ethyl-6-(methylthio)1,3,5-triazin-2,4-diamin) on some biochemical, haematological and histological parameters of the common carp (Cyprinus carpio L.). Two-year-old fish were exposed for 28 days to terbutryn added to the tank water at four concentrations of 0.02 (real environmental concentration in Czech river), 2, 20 and 40 g l−1 . The subchronic exposure of terbutryn in real environmental concentration 0.02 g l−1 had not effect on biochemical, haematological and histopathological profile of common carp. The subchronic exposure of common carp of terbutryn in concentration 2, 20, 40 g l−1 caused significant shifts in biochemical, haematological and histopathological profile. Acknowledgements: This research was supported by the Czech Science Foundation Project No. 525/09/P218, and the USB RIFCH Project No. MSM 6007665809 and the Ministry of the Environment of the Czech Republic SP/2e7/229/07. doi:10.1016/j.toxlet.2009.06.539
Abstracts / Toxicology Letters 189S (2009) S57–S273
Z02 Organochlorine pesticides mixture exposure assessment and DNA damage in mother–child pairs in agricultural community in San Luis Potosi, Mexico ˜ 1 , Regina Montero 2 Diana Alvarado 1,∗ , Leticia Yánez UASLP, Environmental Toxicology, San Luis Potosi, Mexico, 2 UNAM, Genomic Medicine and Environmental Toxicology, Mexico City, Mexico
1
Fifty mother–child pairs from an agricultural community in San Luis Potosí, Mexico were studied, in order to evaluate exposure to organochlorine pesticides mixtures and genotoxic damage, obtaining from them maternal and umbilical cord blood samples. In order to evaluate organochlorine pesticides exposure, 15 pesticides were quantified by using a gas chromatograph electroncapturing detector, and a mass spectrometry detector in maternal as well as in cord plasma. DNA damage was evaluated by comet and clastogenic damage assay. The organochlorine pesticides concentration range in maternal plasma samples was from 5000 to 25,500 ng/g fat. Comet assay was evaluated using olive tail moment (fluorescence intensity and tail length); considering 4 as the reference value, 60% of the mothers, and 78% of the babies manifested damage. In regard to clastogenic damage, this was reported as micronuclei, chromatin buds and nucleoplasmic bridges frequency in every 1000 cells evaluated. For mothers, a range from 0.33 to 5 was obtained, whereas in newborns it was from 0 to 8. The frequency in a non-exposed population is from 0 to 3. The diffusion capacity through placenta of this kind of pollutants was shown, because plasmatic concentrations in the umbilical cord plasma were detected in a range from 9800 to 285,500 ng/g fat. When analyzing the mother’s DNA damage versus the baby’s DNA damage, a statistical significance was observed, not occurring this in clastogenic damage. 84% of the mothers took a folic acid supplement during their pregnancy; it has been reported that this micronutrient has the property of avoiding or repairing DNA damage, which drives us to the hypothesis that folic acid intake might be a crucial fact to avoid genotoxic damage, even though the developing fetus was exposed to organochlorine pesticides, being these results interesting since this kind of population has not been studied in this regard. doi:10.1016/j.toxlet.2009.06.537
Z03
夽 Effects of methiocarb on lipid peroxidation in rat tissues Sibel Özden ∗ , Buket Alpertunga Faculty of Pharmacy, Department of Toxicology, Istanbul, Turkey Methiocarb (3,5-dimethyl-4-(methylthio)phenol methylcarbamate) is an N-methylcarbamate insecticide used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. The aim of this study was to investigate the possible effects of methiocarb to induce lipid peroxidation in tissues of male Wistar rats following of 1-, 5- and 28-day exposures. Animals were divided into six different groups and methiocarb was administered by orally at doses 25, 10 and 2 mg/kg b.w. for 1-, 5- and 28-day, respectively. Liver, kidney, brain and testis tissues were taken from the rats for the biochemical examinations. Lipid peroxidation and reduced
glutathione (GSH) levels were determined in the tissues. Lipid peroxidation was significantly increased in liver, kidney, brain and testis after 1-, 5- and 28-day treatments of methiocarb. GSH levels were significantly increased in 1-day period and significantly decreased in 5- and 28-day periods in all tissues after methiocarb administration. These findings demonstrated that 1-day high dose and 5- and 28-day lower doses treatments of methiocarb may induce lipid peroxidation and have disturbances in the GSH levels in liver, kidney, brain and testis supporting that free radicals may be involved in the mechanism of methiocarb-induced toxicity. Methiocarb-induced toxicity via lipid peroxidation and free radical mechanism has not been previously reported and therefore, this study represents a possible pathway for the mechanism of methiocarb-induced toxicity. Further investigations are required to better understand the mechanisms of oxidative stress in the toxicity of methiocarb. Keywords: Methiocarb; Lipid peroxidation; Glutathione; Liver; Kidney; Brain; Testis 夽 Selected for Oral Presentation. doi:10.1016/j.toxlet.2009.06.538
Z04 Effects of subchronic terbutryn exposure on some biochemical, haematological and histopathological parameters of the common carp (Cyprinus carpio L.) Josef Velisek ∗ , Eliska Sudova, Jana Machova, Zdenka Svobodova University of South Bohemia Ceske Budejovice, Research Institute of Fish Culture and Hydrobiology, Vodnany, Czech Republic S-triazines constitute a group of similar herbicides used extensively in agriculture and non-agricultural use sites, primarily to control broadleaf and some grassy weeds, that have become ubiquitous contaminants of the environment. Due to their heavy use in agriculture and to their persistence, many of these compounds present in surface and ground waters, and have to be considered a potential risk for water life as well as for drinking water quality. The aim of the study was to evaluate subchronic toxic effects of the terbutryn (N-(1,1-dimethylethyl)-N -ethyl-6-(methylthio)1,3,5-triazin-2,4-diamin) on some biochemical, haematological and histological parameters of the common carp (Cyprinus carpio L.). Two-year-old fish were exposed for 28 days to terbutryn added to the tank water at four concentrations of 0.02 (real environmental concentration in Czech river), 2, 20 and 40 g l−1 . The subchronic exposure of terbutryn in real environmental concentration 0.02 g l−1 had not effect on biochemical, haematological and histopathological profile of common carp. The subchronic exposure of common carp of terbutryn in concentration 2, 20, 40 g l−1 caused significant shifts in biochemical, haematological and histopathological profile. Acknowledgements: This research was supported by the Czech Science Foundation Project No. 525/09/P218, and the USB RIFCH Project No. MSM 6007665809 and the Ministry of the Environment of the Czech Republic SP/2e7/229/07. doi:10.1016/j.toxlet.2009.06.539