【摘要】 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。更多还原

【Abstract】 A model test by fed guinea pigs(DHP-Enl sp.)with Keshan disease(KD)endemic cereasls from Yunnan province for 10 weeks,the results have shownthat,the selenium(Se)level and glutathione peroxidase(GSH-Px)activity inplasma,red blood cell(rbc)and myocardial mitochondria in test-animals werelower than that of nonendemic group significantly.The activity of catalase inrbc decreased in some extent.Even the superoxide dismutase activity showed atendency to compensatory increasing,but the levels of conjugated diens andfluorescent chromolipids all the products of peroxidation of membrane lipids byactive oxygen free radicals still increased significatly.The cardiolipin(CL)content and cytochrome c oxidase activity(CCO)inmitochondria of test group were lower than that of control,and its circulardichroism(CD)also abnormal,but the endemic group supplemented with veget-able,in proportion as rising of Se and CL content in tissues the enzymicactivity and CD spectra of mitochondrial CCO were all restored to the normallevel of controls.The CD spectra of mitochondria,submitochondrial particle andCCO all appeared a resemble correspondent changes.Namely,the peak value inendemic cereal groups were all lower significantly。than that of controls.Themolecular pathological mechanism in pathogenesis of KD is discussed in thispaper。更多还原