超氧阴离子对心肌细胞Ca^（2＋）平衡的影响及硒的保护作用  

Change of Ca￣(2+) Homeostasis in Cardiac Myocytes Caused by O￣-_2 and Protective Effect of Se

作　　者：杨志伟[1] 聂玉生[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》1994年第2期196-201,共6页

基　　金：国家"八五"攻关研究课题

摘　　要：在超氧阴离子（Ｏ~－_２）作用下，心肌细胞内游离钙浓度（［Ｃａ^（２＋）］_ｉ）显著升高；心肌细胞膜通透性明显增强；膜脂流动性下降。一定浓度的硒代蛋氨酸（Ｓｅ－Ｍｅｔ）或亚硒酸钠（Ｎａ_２ＳｅＯ_３）可不同程度地拮抗Ｏ~－_２的影响。前者作用更为显著。这两种硒化合物也能提高谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的活性。综上所述，硒缺乏，高自由基及心肌细胞Ｃａ^（２＋）平衡失调三者之间存在着相关性。在Ｏ~－_２作用下，心肌细胞内Ｃａ^（２＋）平衡失调比膜通透性的改变更为敏感。Under the action of O￣-_2, Ca￣(2+)concentration ([Ca￣(2+)_1]i) and membrane permeability of myocardial cells were markedly increased, while the lipid fluidity was decreased. Such change can be antagonized mostly by 1.0 μmol/L selenium methionine (Se-Met) or partly by 2.3 μmol/L Na2SeO3. The O-2 chemiluminescence signal intensity could be significantly quenched by Se-Met or Na2SeO3, but the effect of the former is stronger than the latter. Activity of glutathione peroxidase (GSH-Px) was also increased by both of the Se-containing compounds. There seems to be some interrelationship between Se deficiency, higher active oxygen radicals and the change of Ca￣(2+) homeostasis in the myocardial cells. The change of Ca￣(2+) homeostasis is more sensitive than that of membrane permibility in response to the action of O-2 injury.

关 键 词：超氧阴离子 硒 心肌细胞 钙 克山病 

分 类 号：R362[医药卫生—病理学]