Indexed on: 19 Apr '13Published on: 19 Apr '13Published in: Environmental Toxicology
This study was designed to investigate the possibility of β-cyfluthrin to induce oxidative stress and biochemical perturbations in rat liver and the role of selenium in alleviating its toxic effects. Male Wister rats were randomly divided into four groups of seven each, group I served as control, group II treated with selenium (200 µg/kg BW), group III received β-cyfluthrin (15 mg/kg BW, 1/25 LD50 ), and group IV treated with β-cyfluthrin plus selenium. Rats were orally administered their respective doses daily for 30 days. The administration of β-cyfluthrin caused elevation in lipid peroxidation (LPO) and reduction in the activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR). A decrease in reduced glutathione (GSH) content was also observed. Liver aminotransferases (AST and ALT) and alkaline phosphatase (ALP) were decreased, whereas lactate dehydrogenase (LDH) was increased. Selenium in β-cyfluthrin-induced liver oxidative injury of the rats modulated LPO, CAT, SOD, GSH, GST, GPx, and GR. Also, liver AST, ALT, ALP, and LDH were maintained near normal level due to selenium treatment. It is concluded that selenium scavenges reactive oxygen species and render a protective effect against β-cyfluthrin toxicity.