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

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Abstract

Organophosphate (OP) pesticides such as dimethoate and malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is possible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated orally with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to oral administration of a single low dose of dimethoate and/or malathion (0.01% LD50). The result showed that treatment with OP increased lipid peroxidation (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 erythrocytes from dimethoate and/or malathion treated rats as compared to control 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 protection against OP-induced oxidative stress. The glutathione-S-transferase (GST) activity in erythrocytes was inhibited in OP intoxicated rats which partially recovered in vitamin E pretreated animals administered OP’s. Inhibition 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 vitamin E may amelierate OP-induced oxidative stress by decreasing LPO and altering antioxidant defense system in erthrocytes.

Introduction

Pesticides are occasionally used indiscriminately in large amounts causing environmental pollution and therefore, are a cause of concern. Residual amounts of organochlorines (OC) and organophosphate (OP) pesticides have been detected in the soil, water bodies, vegetables, grains and other foods products [1]. OP are known to cause inhibition of acetylcholinesterase (AChE) activity in the target tissues [2] which accumulates acetylcholine and prevents the smooth transmission of nerve functions leading to convulsions and death. However, low intakes of OP’s through food and water may not show clear symptoms of OP intoxication such as convulsions but it may show mild inhibition of AChE activity in erythrocytes and tissues. Recent studies indicate that dimethoate intoxication produce oxidative stress by the generation of free radicals and induce hepatic LPO in chicken [3] and in mice [4]. As some of the OP’s may be present in blood of exposed humans and animals, it may produce oxidative stress in erythrocytes. The antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) as well as total-SH content in erythrocytes, however, may neutralize the oxidative stress. Vitamin E, a constituent of plasma membrane, is an effective antioxidant and as it is present at the site of free radical generation, it may neutralize the toxic effects of reactive oxygen species (ROS). The rats were thus, pretreated with vitamin E, prior to dimethoate and/or malathion intoxication in order to show whether vitamin E prevents OP-induced oxidative stress in erythrocytes.

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Materials and methods

Male Wistar rats weighing 150–180 g were housed in polypropylene cages under standard conditions with free access to drinking water and basal diet. Rats were selected due to their easy availability as an experimental animal. The animals were regularly weighed. The animals were randomly divided into eight groups each comprising of six animals. The rats were administered orally 0.2 ml. dimethoate and/or malathion (0.01% LD50) as a single dose in 1 ml groundnut oil as vehicle. Groundnut oil was

Lipid peroxidation in erythrocytes

Vitamin E treated rats (group 2) showed erythrocyte LPO comparable to control (Table 1). Treatment with dimethoate and/or malathion (group 3, 5 and 7) showed increased LPO in erythrocytes, as compared to control. Vitamin E pretreated rats administered dimethoate and/or malathion (group 4, 6 and 8) showed significant decrease in erythrocyte LPO as compared to rats administered dimethoate and/or malathion without vitamin E pretreatment (group 3, 5 and 7).

Superoxide dismutase activity in erythrocytes

SOD activity in vitamin E treated rats

Discussion

The results show that treatment with dimethoate and/or malathion produce LPO in erythrocytes. Vitamin E pretreated rats administered dimethoate and/or malathion however, showed decreased LPO in erythrocytes as compared to OP treated rats indicating that it may have beneficial role in lowering OP toxicity. There are no reports to show protective effect of antioxidants in OP toxicity, however, some of the studies have suggested the protective role of antioxidant in OC pesticides, such as

Acknowledgments

The authors thank the University Grants Commission, New Delhi for financial support.

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