Lemasters J J, DiGuiseppi J, Nieminen A L, Herman B
Nature. 1987;325(6099):78-81. doi: 10.1038/325078a0.
Cell surface 'blebbing' is an early consequence of hypoxic and toxic injury to cells. A rise in cytosolic free Ca2+ has been suggested as the stimulus for bleb formation and the final common pathway to irreversible cell injury. Here, using digitized low-light video microscopy, we examine blebbing, cytosolic free Ca2+, mitochondrial membrane potential and loss of cell viability in individual cultured hepatocytes. Unexpectedly, we found that after 'chemical hypoxia' with cyanide and iodoacetate, cytosolic free Ca2+ does not change during bleb formation or before loss of cellular viability. Cell death was precipitated by a sudden breakdown of the plasma membrane permeability barrier, possibly caused by rupture of a cell surface bleb.
细胞表面“起泡”是细胞缺氧和毒性损伤的早期后果。有人提出，胞质游离Ca2+升高是气泡形成的刺激因素，也是不可逆细胞损伤的最终共同途径。在这里，我们使用数字化低光视频显微镜，研究单个培养肝细胞中的气泡形成、胞质游离Ca2+、线粒体膜电位和细胞活力丧失。出乎意料的是，我们发现，在用氰化物和碘乙酸进行“化学性缺氧”后，胞质游离Ca2+在气泡形成期间或细胞活力丧失之前没有变化。细胞死亡是由质膜通透性屏障的突然破坏引起的，这可能是由细胞表面气泡破裂所致。
