OBJECTIVETo determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound.

METHODSAdult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E.

RESULTSExposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage.

CONCLUSIONWe concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.

Acetylcholinesterase ; metabolism ; Animals ; Antioxidants ; administration & dosage ; pharmacology ; Ascorbic Acid ; metabolism ; Biomarkers ; Butyrylcholinesterase ; metabolism ; Dimethoate ; adverse effects ; Glutathione ; metabolism ; Lipid Peroxidation ; drug effects ; Lung Diseases ; diagnosis ; prevention & control ; Oxidative Stress ; Rats ; Rats, Wistar ; Selenium ; administration & dosage ; pharmacology ; Vitamin E ; administration & dosage ; pharmacology