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观察了用克山病病区低硒粮饲养的大鼠心肌、肝、肾、骨骼肌线粒体单胺氧化酶（MAO）活性及肝MAO结构改变。以低硒饲料喂大鼠8～11周后，上述四种组织MAO活性及肝线粒体膜流动性、肝Se含量和谷胱甘肽过氧化物酶活性显著降低。而肝MAO的降解和脂质过氧化物明显增高。喂补硒饲料可防御出现上述改变。在体外肝亚线粒体加硒可防御由脂质过氧化所致的MAO降解。缺Se大鼠不同组织的MAO活性降低差异较大。结果表明硒在防御脂质过氧化及维持MAO结构完整和功能起重要作用。
The activity of mitochondrial MAO and the structure of hepatic MAO in myocardium, liver, kidney and skeletal muscle of rats fed with low and selenium grain in Keshan disease were observed. After being fed with low-selenium diet for 8 to 11 weeks, MAO activity, mitochondrial membrane fluidity, hepatic Se content and glutathione peroxidase activity of the four tissues were significantly decreased. Degradation of liver MAO and lipid peroxides were significantly higher. Feed selenium feed can prevent the above changes. Addition of selenium to liver sub-mitochondria can protect against MAO degradation caused by lipid peroxidation. There was a significant difference in the decrease of MAO activity in different tissues of Se-deficient rats. The results indicate that selenium plays an important role in defense of lipid peroxidation and maintenance of MAO structural integrity and function.