克山病病区粮低Se对大白鼠心肌线粒体Ca转运影响的研究  

Effect of Se Deficiency in Feeds from Keshan disease-Region on Ca Transport of Myocardial Mitockondria from Rat

作　　者：聂玉生[1] 李生广[1] 杨志伟[1] 邢菁如[1] 林治焕[1] 杨福愉[1] 

机构地区：[1]中国科学院生物物理研究所

出　　处：《生物化学杂志》1996年第1期93-98,共6页

基　　金：国家"八五"科技攻关项目

摘　　要：以低Ｓｅ克山病病区粮喂养大白鼠为动物模型，在细胞及亚细胞水平上进行了低Ｓｅ与Ｃａ转运关系的研究，同时测定了线粒体的能量转换功能。结果显示，低Ｓｅ病区粮组动物心肌线粒体Ｃａ转运呈现明显异常，但线粒体能量转换功能尚未发生明显改变。提示线粒体Ｃａ转运功能损伤先于线粒体能量转换功能损伤之前发生。心肌线粒体Ｃａ转运功能可作为更灵敏的指标用于克山病发病机理的研究。上述结果进一步表明克山病是一种“心肌线粒体病”。The effect of Se deficiency in feeds from Keshan disease-region (KDR) on Ca transport of myocardial cells and mitochondria and the relationship between the Ca transport damage and energy transduction damage of mitochondria were investigated with rats. Results show that the mitochondial Ca transport was severely damaged in the low Se diet group,while supplementation of Se in the feeds effectively prevented the damage. The cytosolic free Ca concentration, membrane fluidity and Na+, K + -ATPase activity of myocardial cells,and energy transduction of myocardial mitochondria of the low Se diet group did not change significantly. Theses results suggest that Ca transport damage of myocardial mitochondria may happen before damage of mitochondrial energy transduction ,and status of Ca transport of myocardial mitorhondria is a sensitive parameter for studying the pathogeny of Keshan disease. The mechanisms of role of Se in Keshan disease formation is also discussedf. These results indicate further evidence that 'Keshan disease is a mitochondrial cardiomyopathy', a view suggested by our laboratory in 1986 based on that ultrastructure and oxidative phosphorylation function of mitochondria of Keshan-disease patients were significantly injured.

关 键 词：克山病 硒 线粒体 钙转运 

分 类 号：R542.302[医药卫生—心血管疾病]