内毒素血症时大鼠肝细胞线粒体损伤及其机制的研究

目的:观察急性感染性内毒素血症大鼠肝细胞线粒体呼吸链的损伤及其机制。方法:将体重在250-280g健康SD大鼠随机分为空白对照组、内毒素组。提取内毒素血症大鼠肝细胞线粒体,测定其超氧阴离子O₂生成量,同时测定线粒体呼吸链功能:复合体Ⅱ+Ⅲ的电子传递与质子转移定量关系(H⁺/2e^-)、ADP/O、呼吸控制率(RCR)。结果:内毒素血症大鼠肝细胞线粒体电子漏显著增加;大鼠肝细胞线粒体以琥珀酸为底物的态4和态3呼吸速率增加,ADP/O、RCR及复合体Ⅱ+Ⅲ的H⁺/2e^-显著降低。结论:在内毒素血症的发病机制中存在由于肝细胞线粒体内源性氧自由基生成增加对线粒体呼吸功能所造成的氧化损伤。

Injury of hepatic mitochondria and its pathogenesis in rats with endotoxemia

AIM:To investigate the effect of endotoxin on rat hepatic mitochondria.METHODS:Rats were randomly divided into two groups:endotoxin group and the control. 8 cases of animals were included in each group. The effect of electron leak on the production of endogenous oxygen free radicals and the changes of mitochondria function were studied.RESULTS:Treated with endotoxin, a significant increase in O₂ and the rate of state 3,4 were observed in liver mitochondria; The rate of electron transfer to proton pump of mitochondria respiratory chain complex Ⅱ+Ⅲ(H⁺/2e^-), respiratory control rate and ADP/O decreased significantly.CONCLUSION:A increase in production of endogenous oxygen free radicals induced by endotoxin plays an important role in the injury of rat liver mitochondria.