Frederiks W M, Marx F, Myagkaya G L
Virchows Arch B Cell Pathol Incl Mol Pathol. 1986;51(4):321-9. doi: 10.1007/BF02899041.
Changes in the activity of three mitochondrial enzymes in rat liver after in vitro ischemia have been determined by enzyme histochemical methods. The changes were correlated with the appearance in the electron microscope of flocculent densities in the mitochondria indicative of irreversible cell injury. The flocculent densities were observed in rat liver after about 2 h of ischemia in vitro at 37 degrees C. At the same time the activity of glutamate dehydrogenase, localized in the mitochondrial matrix, started to decrease. However, the activities of succinate dehydrogenase localized in the inner membrane of mitochondria, as well as monoamine oxidase of the mitochondrial outer membrane did not change at that stage. It is concluded from the results of this study and those of others that flocculent densities are formed by denaturation of proteins of the mitochondrial matrix in which glutamate dehydrogenase takes part. It should be considered more as a sign than as the cause of cell death.
采用酶组织化学方法测定了大鼠肝脏在体外缺血后三种线粒体酶活性的变化。这些变化与线粒体中出现的絮状密度相关,这种絮状密度在电子显微镜下表明细胞发生了不可逆损伤。在37℃体外缺血约2小时后,在大鼠肝脏中观察到了絮状密度。与此同时,定位于线粒体基质中的谷氨酸脱氢酶活性开始下降。然而,定位于线粒体内膜的琥珀酸脱氢酶以及线粒体外膜的单胺氧化酶活性在该阶段并未发生变化。从本研究及其他研究结果可以得出结论,絮状密度是由谷氨酸脱氢酶参与的线粒体基质蛋白质变性形成的。它更应被视为细胞死亡的一个标志而非原因。