Carbosulfan-induced oxidative damage following subchronic exposure and the protective effects of N-acetylcysteine in rats.

Carbosulfan (CB)-induced oxidative stress leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. The present study is designed to investigate the preventive effect of N-acetylcysteine (NAC) on carbosulfan-induced hepatic and renal dysfunction in rats. Rats exposed to CB and NAC were examined for toxicity by assessing various biochemical alteration and stress markers including in liver and kidney. Significant increases of blood alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT), creatinine and urea were detected in CB-treated rats. In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) also were assessed. According to the results, rats exposed to carbosulfan showed a significant increase in the accumulation of stress markers and an alteration in the antioxidative enzymes activity, when compared to their respective controls. Interestingly, administration of NAC to CB-treated rats attenuates the toxicity of this compound, objectified by biochemical and oxidative improvement of liver and kidney. Thus, the present study reports for the first time that NAC could be a promising therapeutic agent against CB induced oxidative stress.

Metabolic disorders of acute exposure to malathion in adult Wistar rats.

Malathion is a widely organphosphorus insecticide used in agriculture, which shows strong insecticidal effects. However, the use of this insecticide leads to disruption in metabolic pathways. The aim of this study is to evaluate the acute effects of malathion on metabolic parameters in Wistar rats. Malathion was administered orally to rats at a dose of 400mg/kg body weight dissolved in corn oil. Glucidic and lipidic status were analyzed in plasma, cholinesterase activities were also determined. Malathion induces a transitory hyperglycaemia which correlated with depletion on glycogen content. Plasma triglycerides and LDL level increased significantly in malathion treated-rats. HDL rate was unchanged and cholesterol plasma content decrease transitory but rapidly reached a normal level. Results of this study indicate, clearly, that malathion in acute exposure leads to a disruption of lipid metabolism with an enhancement in LDL and triglyceride contents and may play an important role in the development of atherosclerosis and cardiovascular disease. Disruption in plasma lipid profile may leads to a kind of insulin resistance which results in hyperglycaemia.