Ferrell J E, Huestis W H
Biochim Biophys Acta. 1982 May 7;687(2):321-8. doi: 10.1016/0005-2736(82)90562-4.
Crenation, the shape change that follows ATP depletion in human erythrocytes, also follows ionphore-mediated Ca2+-loading. Experiments designed to test whether Ca2+ mediates metabolic crenation showed that: (1) an influx of extracellular Ca2+ is not required for metabolic crenation; (2) metabolic crenation is accompanied by a 70% increase in 86Rb+ permeability, a change much smaller than the increase expected if crenating concentrations of Ca2+ were released from bound intracellular pools; (3) A23187 plus EGTA, a treatment that depletes intracellular Ca2+ and stops Ca2+ crenation, does not affect metabolic crenation; (4) calmodulin inhibitors do not slow metabolic crenation. We conclude that Ca2+ does not mediate metabolic crenation. Albumin washes reverse Ca2+ crenation and metabolic crenation involve the accumulation of some amphiphilic species (e.g., lysolipid or diacylglycerol) in the cell membrane outer monolayer, and that ATP depletion induces a second crenating process which might be a reorganization of the cytoskeleton.
皱缩是人类红细胞中ATP耗竭后发生的形态变化,在离子载体介导的Ca2+ 加载后也会出现。旨在测试Ca2+ 是否介导代谢性皱缩的实验表明:(1)代谢性皱缩不需要细胞外Ca2+ 的流入;(2)代谢性皱缩伴随着86Rb+ 通透性增加70%,这一变化远小于如果从结合的细胞内池释放出皱缩浓度的Ca2+ 所预期的增加;(3)A23187加EGTA(一种耗尽细胞内Ca2+ 并阻止Ca2+ 皱缩的处理方法)不影响代谢性皱缩;(4)钙调蛋白抑制剂不会减缓代谢性皱缩。我们得出结论,Ca2+ 不介导代谢性皱缩。白蛋白冲洗可逆转Ca2+ 皱缩,代谢性皱缩涉及某些两亲性物质(如溶血脂质或二酰基甘油)在细胞膜外单层中的积累,并且ATP耗竭会引发第二个皱缩过程,这可能是细胞骨架的重组。