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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 mechanism of antimony poisoning liver damage. Methods In this experiment, the model of subacute poisoning was used to observe the effect of antimony trioxide on mitochondrial antioxidant enzymes in mice. Results The anti-antimony trioxide 40 mg / kg daily was injected intraperitoneally for 28 days, and the activities of serum aspartate aminotransferase and alanine aminotransferase were significantly increased in the antimony-contaminated animals. The activity of mitochondrial superoxide dismutase and glutathione peroxidation Compared with the control group, the activity of enzyme in the control group was significantly higher than that in the control group. At 28 days after exposure, the malondialdehyde (MDA) in the mitochondria of antimony-contaminated animals was 4727 ± 121 μmol / L, The difference is very significant. The conclusion shows that the mechanism of antimony induced liver damage is related to its antioxidant capacity and lipid peroxidation.