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标题：Therapeutic effects of N -acetylcysteine against malathion-induced hepatotoxicity
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作者：Heba Mohamed Aboubakr ; Eman Abdelfattah Elzohairy ; Abla Abdelrahman Ali 等
期刊名称：Egyptian Journal of Forensic Sciences
电子版ISSN：2090-5939
出版年度：2019
卷号：9
期号：1
页码：1-9
DOI：10.1186/s41935-019-0142-6
摘要：BackgroundThe 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 pesticide-induced toxicity. The present study was designed to investigate the therapeutic effects of NAC against malathion-induced hepatotoxicity, oxidative stress, genotoxicity, immunotoxicity, inflammation, and acetylcholinestrase alteration in rats. MethodsFour 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.ResultsMalathion 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. ConclusionNAC had therapeutic effects against the detrimental hazards of malathion. Administering NAC to vulnerable risk groups is recommended.
关键词：Malathion; N-acetylcysteine; Hepatotoxicity; Oxidative stress; Genotoxicity; Immunotoxicity; Inflammation