Okayasu T, Curtis M T, Farber J L
Am J Pathol. 1984 Nov;117(2):163-6.
The role of alterations in the cytoskeleton in the anoxic death of cultured hepatocytes was evaluated with the use of cytochalasin B and colchicine. The addition of 50 microM Cytochalasin did, however, reduce the rate of accumulation of dead cells but was without effect on the number of cells that died. After 6 hours of anoxia in the presence of cytochalasin, 80% of the cells were dead. The same number of cells were dead after 4 hours in the absence of cytochalasin. Colchicine was without effect on the cell killing by anoxia. Cytochalasin also did not prevent the increase in the molecular order of the membranes of the anoxic hepatocytes as determined by electron spin resonance spectroscopy. In the presence or absence of cytochalasin, anoxia increased the order parameter, S, of hepatocytes spin-labeled with 12-doxyl stearic acid. These data indicate that changes in the organization of microfilaments that can be prevented by cytochalasin may aggravate the mechanisms mediating the anoxic death of the hepatocytes, but such mechanisms are essentially independent of these alterations in the cytoskeleton. The data do not exclude from a role in anoxic cell death other cytoskeletal changes that may not be affected by either cytochalasin or colchicine.
利用细胞松弛素B和秋水仙碱评估了细胞骨架改变在培养的肝细胞缺氧死亡中的作用。然而，添加50微摩尔的细胞松弛素确实降低了死细胞的积累速率，但对死亡细胞的数量没有影响。在细胞松弛素存在的情况下缺氧6小时后，80%的细胞死亡。在没有细胞松弛素的情况下，4小时后死亡的细胞数量相同。秋水仙碱对缺氧诱导的细胞死亡没有影响。细胞松弛素也不能阻止通过电子自旋共振光谱法测定的缺氧肝细胞膜分子有序性的增加。无论有无细胞松弛素，缺氧都会增加用12-硬脂酰氧基硬脂酸自旋标记的肝细胞的有序参数S。这些数据表明，细胞松弛素可阻止的微丝组织变化可能会加剧介导肝细胞缺氧死亡的机制，但这种机制基本上独立于细胞骨架的这些改变。这些数据并不排除其他可能不受细胞松弛素或秋水仙碱影响的细胞骨架变化在缺氧细胞死亡中起作用。
