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目的探讨胆道梗阻对肝线粒体的损害。方法通过复制犬胆道梗阻模型，动态观察了胆道梗阻不同时相肝线粒体丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）含量及琥珀酸脱氢酶（ＳＤＨ）、细胞素Ｃ氧化酶（ＣＣＯ）活力的变化。结果胆道梗阻２周后肝线粒体ＭＤＡ含量明显升高，而ＳＯＤ含量则明显下降；ＳＤＨ及ＣＣＯ活力均受到明显抑制。线粒体ＭＤＡ与ＳＤＨ，ＣＣＯ变化之间均呈现显著的负相关关系。结论胆道梗阻后肝线粒体受到明显脂质过氧化损害，线粒体呼吸酶受到明显损伤，线粒体脂质过氧化损害是导致线粒体呼吸链损伤的原因之一。
Objective To investigate the damage of bile duct obstruction to liver mitochondria. Methods The mitochondrial malondialdehyde (MDA), superoxide dismutase (SOD) and the activity of succinate dehydrogenase (SDH), cytochrome C oxidase CCO) changes in vitality. Results After 2 weeks of biliary obstruction, the content of MDA in liver mitochondria was significantly increased, while the content of SOD was significantly decreased. The activities of SDH and CCO were significantly inhibited. Mitochondrial MDA and SDH, CCO showed a significant negative correlation between changes. Conclusions The mitochondria of the liver are obviously damaged by lipid peroxidation and the mitochondrial respiratory enzyme is obviously damaged after biliary obstruction. The mitochondrial lipid peroxidation damage is one of the causes of mitochondrial respiratory chain injury.