Genotoxicity associated with oxidative damage in the liver and kidney of mice exposed to dimethoate subchronic intoxication

Abstract

Because of the widespread use of pesticides for domestic and industrial applications, the evaluation of their toxic effects is of major concern to public health. The aim of the present study was to investigate the propensity of dimethoate (DM), an organophosphorus pesticide, to cause oxidative damage in the liver and kidney of mice and its associated genotoxic effect. DM was administered intraperitoneally at doses of 1, 5, 10, 15, and 30 mg/kg body weight for 30 consecutive days in BALB/c mice. Oxidative stress was monitored in the kidney and liver by measuring malondialdehyde level, protein carbonyl concentration, and the catalase activity. The genotoxicity of DM was assessed by the comet assay in vivo. Our results indicated that DM inhibited acetylcholinesterase activities in the liver and kidney of treated mice. DM increased lipid peroxidation and protein carbonyl levels in the liver and kidney in a dose-dependent manner. Catalase activity was found to be significantly increased in the liver and kidney at doses higher than 5 mg/kg body weight. Our study demonstrated that DM induced DNA damage in the liver and kidney of treated mice in a dose-dependent manner; this induction was associated to DM-induced oxidative stress. Further investigations are needed to prove the implication of oxidative stress in genotoxicity induced by DM.