4.7 Article

Oxidative damage, biochemical and histopathological alterations in rats exposed to chlorpyrifos and the antioxidant role of zinc

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PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
卷 96, 期 1, 页码 14-23

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ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.pestbp.2009.08.008

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Chlorpyrifos; Zinc; Oxidative damage; Biochemical and histopathological alterations; Liver and kidneys; Gender; Rats

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The protective effects of zinc on liver and kidney injury induced by chlorpyrifos (CPF) were investigated in rats. Male and female rats were orally administered CPF at a dose of 6.75 mg kg(-1) body weight for 28 consecutive days. An additional CPF group received zinc (227 mg l(-1)) in drinking water throughout the experimental duration. Two groups more served as controls. Administration of CPF resulted in a significant increase in serum lipid peroxidation (LPO) level, while induced significant decreases in the activities of plasma superoxide dismutase (SOD), glutathione-S-transferase (GST) and serum acetylcholinesterase (AChE) either in male or female rats. Similarly, a significant increase in the levels of various serum marker enzymes [e.g. aminotransferases (AST and ALT), lactate dehydrogenase (LDH) and gamma glutamyl transferase (GGT)] and increase the level of total protein, uric acid and creatinine. In contrast, co-administration of zinc to CPF-treated animals restored most of these biochemical parameters to within normal levels. in case of AChE, supplementation of zinc showed little alteration in the activity of this enzyme especially in male rats treated with CPF. CPF caused histopathological change in liver and kidneys of male and female rats. However, zinc administration to CPF-treated animals resulted in overall improvement in liver and kidneys damage, emphasizing its antioxidant role. In light of the available data, it can deduce that CPF-induced lipid peroxidation, oxidative stress, liver and kidneys damage in male and female rats, and conjunction supplementation of zinc has resulted in pronounced ameliorating effect. (c) 2009 Elsevier Inc. All rights reserved.

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