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经过多年研究证明克山病是一种以心肌线粒体膜损害为主要特征的地方性心肌病,这次通过用克山病区低硒粮模拟病区居民生活喂养幼豚鼠15周,结果发现血及心、肝等组织,线粒体、微粒体及上清中的硒水平及谷胱甘肽过氧化物酶活性下降,谷胱甘肽转硫酶活性未见升高,甚而降低。脂质过氧化物、氢过氧化物及荧光色脂增加,线粒体膜脂中的心磷脂减少,同时线粒体内膜结合酶的细胞色素氧化酶(CCO)活性下降,即出现了膜的氧化损伤和膜功能障碍。在向提纯的 CCO 中加心磷脂的重组复性试验中实现了 CCO 活性的明显增加,可见线粒体膜结构与功能的异常是克山病患者心肌能量代谢障碍乃至心肌坏死等病理改变的基础。
After years of research shows that Keshan disease is a myocardial mitochondrial membrane damage characterized as endemic cardiomyopathy, this time by using Keshan ward low selenium diet simulated sick area residents living young guinea pigs 15 weeks and found that blood and Heart, liver and other tissues, mitochondria, microsomes and supernatant selenium levels and glutathione peroxidase activity decreased, glutathione S-transferase activity did not increase, or even lower. Lipid peroxides, hydroperoxides, and fluorescent color lipids increased, cardiolipin decreased in mitochondrial membrane lipids, and mitochondrial membrane-bound enzyme cytochrome oxidase (CCO) activity decreased, that is, oxidative damage to the membrane and Membrane dysfunction. CCO activity was significantly increased in recombinant refolding experiments of cardiolipin in purified CCOs. The abnormalities in mitochondrial membrane structure and function were the basis of pathological changes of myocardial energy metabolism and myocardial necrosis in Keshan disease.