Dahl C E, Levine R P
Proc Natl Acad Sci U S A. 1978 Oct;75(10):4930-4. doi: 10.1073/pnas.75.10.4930.
Sheep erythrocytes have been spin labeled with 5-, 12-, and 16-nitroxystearic acid in order to investigate complement-induced changes in the physical state of the lipid bilayer. Formation of osmotic lesions in the membrane causes an increase in the fluidity of the membrane which overcomes the decrease in membrane fluidity caused by the interaction of the complement proteins. A decrease in membrane fluidity is observed only when complement-lysed membranes are resealed or when complement proteins react with isosmolar ghosts that do not undergo osmotic lysis. The decrease in bulk fluidity of the membrane is first observed when C8 binds to the membranes bearing C5b67 and is enhanced upon the subsequent binding of C9. The decrease in membrane fluidity shown by the electron spin resonance spectra of spin-labeled fatty acids suggests that certain of the complement proteins penetrate the membrane and interact with hydrophobic regions of the lipid bilayer.
为了研究补体诱导的脂质双层物理状态变化,已用5-、12-和16-硝基硬脂酸对绵羊红细胞进行自旋标记。膜中渗透损伤的形成会导致膜流动性增加,这克服了补体蛋白相互作用引起的膜流动性降低。仅当补体裂解的膜重新封闭时,或当补体蛋白与不发生渗透裂解的等渗血影反应时,才观察到膜流动性降低。当C8与带有C5b67的膜结合时,首先观察到膜整体流动性降低,随后C9结合后这种降低会增强。自旋标记脂肪酸的电子自旋共振光谱显示的膜流动性降低表明,某些补体蛋白穿透膜并与脂质双层的疏水区域相互作用。