Krähenbühl S, Reichen J
Dept. of Internal Medicine, University of Berne, Switzerland.
Scand J Gastroenterol Suppl. 1992;193:90-6. doi: 10.3109/00365529209096012.
Mitochondrial function and structure in cirrhotic livers from humans or rats show a variety of changes as compared to control livers. Mitochondrial ATP production is reduced in rats with CCl4- or thioacetamide-induced liver cirrhosis and in rats with secondary biliary cirrhosis. Activity of the electron transport chain is decreased in rats with secondary biliary cirrhosis. In rats with CCl4-induced cirrhosis, the mitochondrial content of certain constituents of the respiratory chain (cytochrome a + a3, cytochrome b and ubiquinone) is increased and activities of cytochrome c oxidase and ATPase are elevated. Similarly, in humans with liver cirrhosis, mitochondrial cytochrome a + a3 content is elevated and has been used to assess the risk for hepatectomy. In rats with secondary biliary cirrhosis, compensatory strategies include increased mitochondrial volume per hepatocyte and possibly increased extramitochondrial ATP production (increased glycolysis). Thus, a variety of adaptive mechanisms are used to maintain mitochondrial function in cirrhotic livers.
与对照肝脏相比，人类或大鼠肝硬化肝脏中的线粒体功能和结构呈现出多种变化。在四氯化碳或硫代乙酰胺诱导的肝硬化大鼠以及继发性胆汁性肝硬化大鼠中，线粒体ATP生成减少。继发性胆汁性肝硬化大鼠的电子传递链活性降低。在四氯化碳诱导的肝硬化大鼠中，呼吸链某些成分（细胞色素a + a3、细胞色素b和泛醌）的线粒体含量增加，细胞色素c氧化酶和ATP酶的活性升高。同样，在肝硬化患者中，线粒体细胞色素a + a3含量升高，并已被用于评估肝切除风险。在继发性胆汁性肝硬化大鼠中，代偿策略包括每个肝细胞的线粒体体积增加以及可能增加线粒体外ATP生成（糖酵解增加）。因此，多种适应性机制被用于维持肝硬化肝脏中的线粒体功能。
