Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.5.1.18 (glutathione S-transferase)
 22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the acute toxicity of the pesticide methomyl on the topmouth gudgeon (Pseudorasbora parva) was evaluated using mortality and the activity of the enzymes acetylcholinesterase (AChE), glutathione S-transferases (GSTs), glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) as endpoints. LC50 values were 1.228, 0.782, 0.538, and 0.425 mg/l at 24, 48, 72, and 96 h of exposure, respectively. Methomyl caused a sharp decrease in specific activity of brain AChE around 48% at concentrations between 0.043 and 0.213 mg/l. A reduction higher than 40% in liver GST activity at concentrations between 0.085 and 0.213 mg/l was found, whereas no significant effects were observed in intestinal GST. A significant concentration-dependent decrease of GOT activity was found after 24 h of exposure to the pesticide but not after 96 h. No significant effects on GPT activity were observed. These results indicate that at the concentrations tested, methomyl is acutely toxic to the species P. parva, causing mortality, neurotoxic effects, and changes in some hepatic enzymes.
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PMID:Acute toxicity of the pesticide methomyl on the topmouth gudgeon (Pseudorasbora parva): mortality and effects on four biomarkers. 1866 58

The widespread of pesticide in public health and agriculture has caused severe environmental pollution and health hazards. Methomyl is used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. In this study, we aimed to investigate the effects of methomyl at different time intervals on lipid peroxidation, reduced glutathione (GSH), total sulfhydryl group (T-SH), antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and histopathological changes in mice kidney. Ten CD-1 mice per group were assigned to one of four treatment groups. Group one served as control while groups 2, 3 and 4 were orally treated with 1mgmethomyl/kg BW for 10, 20 and 30 days, respectively. Methomyl significantly increased lipid peroxidation in kidney as compared to control group. Levels of GSH and T-SH and activities of SOD, CAT and GST were found to be decreased. On the other hand, methomyl significantly increased the levels of urea, uric acid and creatinine in serum. The histological examination of kidney revealed damage involving the entire renal nephrons in both 20 and 30 days of methomyl exposure. Severe dilatation of the cortical tissue, congested glomerulus with swelling of the endothelial cells and degeneration of the epithelium cells lining the tubules were observed. In conclusion, the results suggest that methomyl exposure can cause renal damage, oxidative stress, perturbations in antioxidant defense system and histopathologic changes in mice kidney in a time dependent manner.
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PMID:Kidney antioxidant status, biochemical parameters and histopathological changes induced by methomyl in CD-1 mice. 2337 92