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动物实验结果表明半合成低硒饲料不足以引起心肌线粒体超微结构与内膜氧化磷酸化功能的明显变化;喂以克山病病区粮能引起心肌线粒体超微结构与能量转换功能明显的异常,但与克山病患者心肌线粒体损伤的程度比较尚有一定距离,病区粮补 Se 能明显减轻线粒体一系列的异常,这说明了克山病的形成低 Se 只是一个重要条件,尚有其它综合因素的参与,同时也在细胞分子水平上进一步肯定了 Se 对克山病的预防作用。
Animal experiments show that semi-synthetic low-selenium feed is not enough to cause myocardial mitochondrial ultrastructure and intimal oxidation and phosphorylation of significant changes; fed with Keshan disease grain can cause myocardial mitochondrial ultrastructure and energy conversion was significantly abnormal , But with Keshan disease in patients with myocardial mitochondrial damage compared to the extent there is still a certain distance, the wards grain Se Se can significantly reduce a series of mitochondrial abnormalities, indicating Keshan disease is a low Se formation is an important condition, there are other Comprehensive factors involved, but also at the molecular level to further affirmed Se Keshan disease prevention.