Dimethoate

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% LD 50 ). 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.

Abstract: The main objective of the present study was to investigate if a battery of enzymatic biomarkers was suitable for use as effect criteria in acute toxicity tests with Poecilia reticulata. To attain this objective, the in vivo effects of dimethoate and beta-naphthoflavone on acetylcholinesterase (AChE), cytochrome P4501A-dependent monooxygenase activity of 7-ethoxyresorufin O-deethylase (EROD), glutathione S-transferases (GST), lactate dehydrogenase (LDH) and Na+-K+-ATPase activities of P. reticulata were studied. After 96 h of exposure to sublethal concentrations (0.063 mg l−1 to 1 mg l−1) of the pesticide, an inhibition of the enzymes AChE and GST, as well as an induction of LDH was observed. The compound beta-naphthoflavone significantly induced both EROD and GST. The remaining enzymes analysed were not significantly altered by the exposure to beta-naphthoflavone (0.82 mg l−1 to 1.7 mg l−1). These results suggest that in vivo toxicity tests based on the biomarkers used in this study are sensitive and present advantages to conventional acute tests based on mortality, since they were able to detect sublethal effects in a short-period of time (96 h) indicating target and/or detoxification mechanisms.