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

OBJECTIVEThe present study investigated the protective role of Hyparrhenia hirta (H. hirta) against sodium nitrate (NaNO3)-induced hepatoxicity.

METHODSMale Wistar rats were randomly divided into three groups: a control group and two treated groups during 50 d with NaNO3 administered either alone in drinking water or co-administered with H. hirta.

RESULTSNaNO3 treatment induced a significant increase in serum levels of glucose, total cholesterol and triglyceride while serum total protein level decreased significantly. Transaminases and lactate deshydrogenase activities in serum were elevated indicating hepatic cells' damage after treatment with NaNO3. The hyperbilirubinemia and the increased serum gamma glutamyl transferase activities suggested the presence of cholestasis in NaNO3 exposed rats. In parallel, a significant increase in malondialdehyde level along with a concomitant decrease in total glutathione content and superoxide dismutase, catalase and glutathione peroxidase activities were observed in the liver after NaNO3 treatment. Furthermore, nitrate caused a significant induction of DNA fragmentation. These modifications in NaNO3-treated rats corresponded histologically with hepatocellular necrosis and mononuclear cells infiltration. H. hirta supplementation showed a remarkable amelioration of the abnormalities cited above.

CONCLUSIONThe results concluded that the treatment with H. hirta had a significant role in protecting the animals from nitrate-induced liver dysfunction.

Animals ; Chemical and Drug Induced Liver Injury ; prevention & control ; DNA Fragmentation ; drug effects ; Drug Evaluation, Preclinical ; Eating ; drug effects ; Flavonoids ; analysis ; Glutathione ; drug effects ; Lipid Peroxidation ; drug effects ; Lipids ; blood ; Liver ; drug effects ; metabolism ; pathology ; Male ; Mice ; Nitrates ; Organ Size ; drug effects ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Poaceae ; chemistry ; Random Allocation ; Rats, Wistar