Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes

Organophosphate (OP) pesticides such as dimethoate and malathion intoxicati on has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is p ossible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated ora lly with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to o ral administration of a single low dose of dimethoate and/or malathion (0.0 1% LD50). The result showed that treatment with OP increased lipid peroxida tion (LPO) in erythrocytes, however, vitamin E pretreated rats administered OP's showed decreased LPO in erythrocytes. The increase in the activities of superoxide dismutase (SOD) and catalase (CAT) and total-SH content in er ythrocytes from dimethoate and/or malathion treated rats as compared to con trol appears to be a response towards increased oxidative stress. Vitamin E pretreated animals administered OP's showed a lowering in these parameters as compared to OP treated rats which indicates that vitamin E provide prot ection against OP-induced oxidative stress. The glutathione-S-transferase ( GST) activity in erythrocytes was inhibited in OP intoxicated rats which pa rtially recovered in vitamin E pretreated animals administered OP's. Inhibi tion in erythrocyte and serum acetylcholinesterase (AChE) activity was not relieved in vitamin E pretreated rats administered OP's probably due to the competitive nature of enzyme inhibition by OP's. The results show that vit amin E may amelierate OP-induced oxidative stress by decreasing LPO and alt ering antioxidant defense system in erthrocytes. (C) 2001 Elsevier Science Inc. All rights reserved.