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用黄嘌呤-黄嘌呤氧化酶体系或低硒饲料诱发自由基损伤。在培养的鼠心肌细胞上,硒能使受损心肌细胞的自由基含量、超微结构、动作电位、膜输入阻抗恢复正常;在离体灌流的鼠心上,硒能改善受损心脏的心肌收缩性能;硒能使受损鼠的心硒含量与肝谷胱甘肽过氧化物酶(GSH_(ps))活力回升、肝过氧化脂质(LPO)含量下降。上述结果提示硒保护作用的基本机制可能与增强GSH_(px)活力、促进自由基清除有关。
Free radical damage induced by xanthine - xanthine oxidase system or low selenium diet. Selenium can restore the free radical content, ultrastructure, action potential and membrane input impedance of injured myocardial cells in cultured rat cardiomyocytes. Selenium can improve myocardial damage in isolated heart Selenium could make heart selenium content and hepatic glutathione peroxidase (GSH_ (ps)) activity of injured rats recover, and the content of LPO decreased. The above results suggest that the basic mechanism of selenium protection may be related to enhancing GSH px activity and promoting free radical scavenging.