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作 者:王安[1] 安飞云[1] 高泽宣[1] 王夷平[1]
机构地区:[1]湖南医科大学环境医学研究室
出 处:《中华预防医学杂志》1998年第4期229-230,共2页Chinese Journal of Preventive Medicine
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40mg/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4727±121μmol/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。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 antioxidase 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 antioxidation and lipid peroxidation in the liver mitochondria.
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