Se和V_E与克山病

以克山病病区粮配成基础饲料，另在基础饲料中分别补充Ｓｅ或ＶＥ，或Ｓｅ＋ＶＥ喂养大鼠，在细胞及亚细胞水平上以Ｃａ代谢为主研究并比较了Ｓｅ和ＶＥ在克山病病因中的作用。测量了心肌细胞和心肌线粒体的Ｃａ代谢及有关指标、心肌线粒体能量转换功能及心肌组织自由基含量。结果表明，在低Ｓｅ病区粮中补充Ｓｅ或ＶＥ均能在一定程度上预防病区粮中致病因素对心肌细胞及线粒体的损伤；并且补充Ｓｅ或ＶＥ均能使心肌组织中自由基含量减少。提示Ｓｅ和ＶＥ是通过清除体内过量自由基预防细胞和线粒体的损伤的。但值得注意的是，实验中所用病区粮ＶＥ含量不低于甚至高于非病区对照粮，在低Ｓｅ情况下，所补ＶＥ的量需要相当大（如本实验中补充２００μｇ／ｇ）才能较明显地预防心肌细胞和心肌线粒体的损伤。通过对这些结果的分析，进一步肯定低Ｓｅ是克山病形成的重要因素之一。

Se, V_E AND PATHOGENY OF KESHAN DISEASE

The roles of Se and VE, related to the pathogeny of keshan Disease were investigated and compared each other at Cellular and subcellular levels, with stress on the Ca2 homeostasis. The experimental rats were fed diet from Keshan-Disease-Region(KDR) with or without supplementation of Se/VE. The criteria measured were as follows: Ca2 transport of myocardial Cells and chchondria, effidricy of energy tthnsduCtion of myocardial Antochondria and free radical in myocardium. Results shoWed that the KDR diet with low-Se content caused damage to myocaridial Cells and chchondria. When the diet was supplemented with Se/ VE all the abnormalttities mentioned above were ndutal tO a certain extant, and the level of the free radical of myocardium were decreased signfficantiy. It suggested that the preventive effect of Se and Vs affected through scavenging the excess amount of free radical. However, it should be notal that the VE content of the KDR diet is not lower than the control's but dosage of Vs needed to prevent the damages is quite large in the case of low Se state (e. g. 200ppm was adde into the KDR diet in our experiments). These results ftirther demonstrate that lack of Se is an important factor for the pathogeny of Keshan Disease.