Methomyl induced hematological and biochemical alterations - protection by vitamin E

The present study was planned to evaluate the role of vitamin E, if any, in attenuating the methomyl induced hematological and biochemical alterations in blood of male wistar rats. Animals, in the weight range of 130-150 g, were administered methomyl orally in drinking water at a sub-acute dose level of 4 mg/kg body weight on alternate days for a duration of one month, vitamin E was administered intraperitoneally to normal or methomyl treated rats on alternate days as a pretreatment for a week at a dose level of 50 mg/kg body weight and subsequently for a further period of one month. Methomyl treatment resulted in a significant increase in the levels of lipid peroxidation and super oxide dismutase (SOD) activity in erythrocytes. On the contrary, reduced Glutathione levels (GSH) and the activities of catalase, Glutathione-S-transferase (GST) and Glutathione peroxidase (GSHPx) were found to be significantly decreased. Methomyl treatment caused a significant increase in total leukocyte counts (TLC), platelet, neutrophil, eosinophil, and lymphocyte and monocyte counts. Scanning Electron Micrographs showed significant morphological changes, which included spherocytosis and poikilocytosis. However, vitamin E supplementation to methomyl treated rats significantly decreased the raised levels of LPO whereas it caused a significant increase in GSH levels. Also, vitamin E supplementation could significantly elevate the activities of catalase GSHPx, GST and resulted in the normalization of SOD activity. Vitamin E supplementation also proved to be effective in significantly decreasing the already raised values of TLC and lymphocytes counts and almost normalized the platelets, neutrophils, lymphocytes and monocytes counts. Further, vitamin E supplementation improved the morphology of the red blood cells. The study, therefore, concludes that vitamin E can effectively mitigate most of the adverse effects induced by methomyl in rat blood. (c) 2009 Elsevier Inc. All rights reserved.