Toxic Effects of Lead Exposure in Rats: Involvement of Oxidative Stress, Genotoxic Effect, and the Beneficial Role of N-Acetylcysteine Supplemented with Selenium

Abstract

This study was carried out to investigate the in vivo protective role of N-acetylcysteine (NAC) per se, along with selenium (Se), against lead-induced hepatic, nephritic-oxidative, and neuronal-oxidative damage in rats. Lead acetate at a dose of 50 mg/kg body weight administered intraperitoneally for 3 days was preferred as the source of lead. Various oxidative stress markers such as reduced glutathione content, lipid peroxidation, superoxide dismutase, and catalase were measured to determine the degree of oxidative damage and healing due to NAC (50 mg/kg body weight administered orally) and Se (0.5 mg/kg body weight administered orally) and were studied along with the activities of enzymes such as transaminases (aspartate aminotransferase/alanine aminotransferase), δ-aminolevulinic acid dehydratase, δ-aminolevulinic acid synthase, and acetyl cholinesterase activity. The genotoxic effect of lead also was studied in terms of DNA damage using comet assay. The effect of lead was studied in blood biochemical variables such as cholesterol, triglycerides, urea, uric acid, and creatinine. Our data suggest that supplementation of Se with NAC can improve the lead-induced biochemical oxidative stress in blood and tissue, the burden of lead on the body, and molecular alterations by recoupment in mean DNA damage.