Inouye B, Aono K, Iida S, Utsumi K
Physiol Chem Phys. 1979;11(2):151-60.
During studies of the mechanism by which hemolysis is induced in irradiated human erythrocytes in vitro, several inducements of membrane lipid peroxidation and protective effects of vitamin E (V.E) and superoxide dismutase (SOD) were investigated. Findings were: (1) Before hemolysis, K+ release from erythrocytes induced by radiation stimulated hemolysis but was inhibited by V.E or SOD. (2) Lipid peroxidation of mitochondria induced by Fe3+, ADP, and superoxide (O2-) generating system, and lipid peroxidation of microsome induced by O2- generating system, were also inhibited by V.E or SOD. (3) X-ray or 60Co gamma-ray radiation stimulated lipid peroxidation of liver homogenate, microsome, and liposome. Some of this peroxidation was inhibited by V.E. or SOD. These results suggest that O2- and/or OH formation by radiation induces membrane lipid peroxidation, which causes deterioration of membrane resulting in change of ion permeability and consequent hemolysis.
在对体外照射人红细胞诱导溶血机制的研究过程中,研究了几种膜脂质过氧化的诱导因素以及维生素E(V.E)和超氧化物歧化酶(SOD)的保护作用。研究结果如下:(1)溶血前,辐射诱导的红细胞钾离子释放会刺激溶血,但会被V.E或SOD抑制。(2)由Fe3+、ADP和超氧化物(O2-)生成系统诱导的线粒体脂质过氧化,以及由O2-生成系统诱导的微粒体脂质过氧化,也会被V.E或SOD抑制。(3)X射线或60Coγ射线辐射会刺激肝匀浆、微粒体和脂质体的脂质过氧化。这种过氧化作用的一部分会被V.E或SOD抑制。这些结果表明,辐射产生的O2-和/或OH会诱导膜脂质过氧化,导致膜结构恶化,从而改变离子通透性并引发溶血。