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锑对小鼠肝线粒体抗氧化酶系统影响的实验研究 |
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王安 安飞云 高泽宣 王夷平
【摘要】 目的 探讨锑中毒性肝损害的机理。方法 本实验以亚急性中毒实验模型，观察了三氧化二锑对小鼠肝线粒体抗氧化酶的影响。结果 每天腹腔注射40 mg/kg三氧化二锑28天，染锑动物血清天冬氨酸氨基转移酶和丙氨酸氨基转移酶活性明显增高；肝线粒体超氧化物歧化酶和谷胱甘肽过氧化物酶的活性与对照组比较，差异有显著性；与对照组相比，染毒28天时，染锑组动物肝线粒体丙二醛为47.27±1.21 μmol/L，与对照组比较，差异有极显著性。结论 表明锑引起肝损害的机理与其损伤肝线粒体的抗氧化能力，产生脂质过氧化作用有关。
【关键词】 锑 肝线粒体 超氧化物歧化酶 谷胱甘肽过氧化物酶 丙二醛
An Experimental Study on Effects of Antimony on Anti-oxidase System on Liver Mitochondria in Mice Wang An, An Feiyun, Gao Zexuan, et al. Department of Environmental Medicine, Hunan Medical University, Changsha 410078
【Abstract】 Objective To explore the mechanisms of toxic liver damage caused by antimony. Methods Experimental mice were injected peritoneally 40 mg/kg of antimony trichloride daily for 28 days to observe the effects of it on the anti-oxidase system in their liver mitochondria. Results Activities of aspartate aminotransferase and alanine aminotransferase increased obviously in the experimental animals, and those of superoxide dismutase and glutathione peroxidase in liver mitochondria lowered, as compared to those in the control animals with statistical significance. Content of malonyl dialdehyde in the liver mitochondria was 47.27±1.21 μmol/L in the experimental animals, significantly higher than that in controls. Conclusion It suggested that the mechanism of liver damage caused by antimony associated with injury to the ability of anti-oxidation and lipid peroxidation in the liver mitochondria.
【Key words】 Antimony Liver mitochondria Superoxide dismutase Glutathione peroxidase Malonyl dialdehyde
锑是制造合金的重要金属，金属锑及其化合物属亲肝性化合物，锑可在肝脏蓄积，造成肝脏损害［1］。职业性锑中毒患者可见明显肝肿大和血清丙氨酸氨基转移酶(ALT)活性增加［2］，游离肝细胞培养表明金属锑具有明显的肝细胞毒性［3］，有关锑中毒性肝损害的毒作用机理尚未完全阐明。本实验采用小鼠腹腔注射三氧化二锑，观察在锑中毒性肝损害过程中，肝线粒体中具有过抗氧化作用的超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的变化和脂质过氧化作用，为探讨锑中毒性肝损害的机理提供依据。
材料与方法
1.实验动物分组与染毒：本校实验动物中心提供的健康昆明小鼠40只，雌雄各半，体重15～20 g，随机分为锑染毒组和对照组，每组20只[1] [2] 下一页
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