羟自由基诱导心肌细胞损伤时ATP酶等变化

Changes of Ca^(2+),Mg^(2+)-ATPase etc in cardiomyocytes damages induced by hydroxyl free radicals

目的 探讨外源性羟自由基诱导乳鼠心肌细胞损伤的作用机理。方法 采用 Fe SO4 / H2 O2 产生系统 ,羟自由基诱导心肌细胞损伤 ,观察乳鼠心肌细胞内 Na+、K+ - ATP酶 ,Ca2 +、Mg2 + - ATP酶和丙二醛 (MDA)含量及其上清液中乳酸脱氢酶 (L DH)与一氧化氮 (NO)含量变化。结果 心肌细胞中 Na+、K+ - ATP酶 ,Ca2 +、Mg2 + - ATP酶减少 ,MDA含量增加 ,与对照组相比较 ,具有显著性差异 (P<0 .0 1,P<0 .0 5 ,P<0 .0 1) ;上清液中 L DH和 NO漏出增加 ,与对照组相比较 ,均具有显著性差异 (P<0 .0 1)。结论 羟自由基诱导心肌细胞中 Na+ 、K+ - ATP酶 ,Ca2 + 、Mg2 + - ATP酶减少 ,MDA及其上清液中 L DH和 NO漏出增加。从而揭示外源性羟自由基可能通过增加膜脂质过氧化 ,引起 ATP酶失活及膜结构破坏等 。

Objective To investigate the mechanism of cardiomyocytes damages induced by exogenouse hydroxyl free radicals in neonatal rat. Methods Damages of cardiomyocytes were induced by hydroxyl free radicals, which were produced by FeSO 4/H 2O 2 system. The following parameters were observed: Na +,K +-ATPase, Ca 2+,Mg 2+-ATPase and MDA in cardiomyocytes, LDH and NO in culture supernatants.Results The volume of Na +,K +-ATPase and Ca 2+,Mg 2+-ATPase were singnificantly decreased in cardiomyocytes damages of neonatal rat(P< 0.01,P<0.05 vs controls). In addition, the volume of MDA in cardiomyocytes, LDH and NO in culture supernatants were singnificantly increased (P<0.01, P<0.01, P<0.01). Conclusion Hydroxyl free radicals can decrease the volume of ATP-ase in cultured cardiomyocytes and can increase the volume of MDA in cultured cardiomyocytes and leakage of LDH and NO in culture supernatants. This diclosed that exogenouse hydroxyl free radicals rise to devitalization of ATPase and damage the structure of meamberane through increasing membrane lipid peroxidation approximately, and is one of reasons caused to cardiomyocytes dealth.