Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9034886 | Toxicology | 2005 | 9 Pages |
Abstract
Dimethoate, an organophosphate pesticide, is used in controlling the pests of a variety of crops. The study was carried out to understand the role of dimethoate in inducing oxidative stress leading to generation of free radicals and alterations in antioxidant enzymes and scavengers of oxygen free radicals. The effects of subchronic exposure of dimethoate in the production of oxidative stress were evaluated in male Wistar rats in the present study. Dimethoate was administered orally at doses 0.6, 6, and 30Â mg/kg for 30 days in these rats. The results indicated an increase in levels of hepatic Cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver and brain at doses 6 and 30Â mg/kg. There were no significant changes in the level of glucose-6-phosphate dehydrogenase activity except in liver at 30Â mg/kg. A decrease in glutathione was observed at 30 and 6Â mg/kg in both liver and brain. Glutathione-S-transferase increased at 30 and 6Â mg/kg in liver and 30Â mg/kg in brain. Erythrocyte acetylcholinesterase was inhibited at 30 and 6Â mg/kg doses. Dose-dependent histopathological changes were seen in both liver and brain. This study concludes that oxidative stress due to dimethoate may be ascribed to induction of Cytochrome P450, inhibition of AChE and disturbance in activities of GSH and GST enzymes causing lipid peroxidation and histological and electron microscopic changes in liver and brain.
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Authors
Yukti Sharma, Somia Bashir, M. Irshad, T.C. Nag, T.D. Dogra,