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克山病区粮喂养豚鼠10周,可见其血浆、红细胞及心肌线粒体中的硒和谷胱甘肽过氧化物酶活性明显降低,红细胞膜过氧化氢酶活性降低,超氧化物歧化酶活性趋向增加,膜脂受氧自由基作用产生的共轭双烯、荧光色脂明显增加,表明存在膜的氧化损伤。实验组心肌线粒体中的心磷脂(CL)减少,细胞色素氧化酶(CCO)活性降低,园二色性(CD)异常,而补充青菜组随 CL 的增加,可见其 CCO 酶活性,CD 谱均恢复到接近正常水平,各实验组心肌线粒体、亚线粒体及纯化 CCO 的 CD 谱异常,峰值(208及224nm)明显低于对照,说明其线粒体 CCO 构象出现了异常。文中讨论了克山病发病的分子病理机制。
Keshan ward feed grain for 10 weeks, showing that the plasma, erythrocyte and myocardial mitochondrial selenium and glutathione peroxidase activity was significantly reduced, erythrocyte membrane catalase activity decreased, superoxide dismutase activity trend Increase, the membrane lipid by the oxygen free radicals generated conjugated diolefin, fluorescent color lipids increased significantly, indicating the existence of membrane oxidative damage. Cardiac mitochondria in the experimental group showed a decrease in cardiolipin (CL), a decrease in cytochrome oxidase (CCO) activity and an abnormal dichroism (CD) in the mitochondria of the experimental group, while the CCO activity and the CD spectrum (P <0.05). The CD spectra of mitochondria, mitochondria and purified CCO in each experimental group were abnormal and their peaks (208 and 224 nm) were significantly lower than that of the control, indicating that their mitochondrial CCO conformations were abnormal. The article discusses the molecular pathogenesis of Keshan disease.