No abstract

Background: The wide unregulated use of malathion has produced severe health hazards. N-acetylcysteine (NAC) is a known glutathione precursor, and there is a growing attention concerning its beneficial effects against pesticideinduced toxicity. The present study was designed to investigate the therapeutic effects of NAC against malathioninduced hepatotoxicity, oxidative stress, genotoxicity, immunotoxicity, inflammation, and acetylcholinestrase alteration in rats. Methods: Four groups comprised of 25 male rats each. Group 1 received distilled water, group 2 received NAC 150 mg/kg/day, group 3 received malathion 50 mg/kg/day, and group 4 received malathion 50 mg/kg/ day followed by NAC 150 mg/kg/day for 90 consecutive days. Aspartate transaminase; alanine transaminase; alkaline phosphatase and lactate dehydrogenase; lipid peroxidation; reduced glutathione and total antioxidant capacity; DNA fragmentation; apoptosis and antiapoptosis-related gene expression; leukocyte counts; myeloperoxidase and immunophenotyping of CD4+ and CD8+; interleukin-1β, interleukin-6, and interferon-γ expression; and acetylcholinestrase were assessed. Results: Malathion administration resulted in significant hepatic injury, immunotoxicity, genotoxicity, oxidative stress injury, inflammation, and significant reduction in acetylcholinestrase activity. Furthermore, malathion showed damaging histopathological effects on liver tissue. NAC treatment significantly attenuated all the previously mentioned biochemical, molecular, and histopathological alterations induced by malathion. Conclusion: NAC had therapeutic effects against the detrimental hazards of malathion. Administering NAC to vulnerable risk groups is recommended.