Muldrew K, McGann L E
Department of Pathology, University of Alberta, Edmonton, Canada.
Biophys J. 1990 Mar;57(3):525-32. doi: 10.1016/S0006-3495(90)82568-6.
The phenomenon of intracellular freezing in cells was investigated by designing experiments with cultured mouse fibroblasts on a cryomicroscope to critically assess the current hypotheses describing the genesis of intracellular ice: (a) intracellular freezing is a result of critical undercooling; (b) the cytoplasm is nucleated through aqueous pores in the plasma membrane; and (c) intracellular freezing is a result of membrane damage caused by electrical transients at the ice interface. The experimental data did not support any of these theories, but was consistent with the hypothesis that the plasma membrane is damaged at a critical gradient in osmotic pressure across the membrane, and intracellular freezing occurs as a result of this damage. An implication of this hypothesis is that mathematical models can be used to design protocols to avoid damaging gradients in osmotic pressure, allowing new approaches to the preservation of cells, tissues, and organs by rapid cooling.
通过在低温显微镜上对培养的小鼠成纤维细胞进行实验设计，研究了细胞内结冰现象，以严格评估目前描述细胞内冰形成的假说：(a) 细胞内结冰是临界过冷的结果；(b) 细胞质通过质膜上的水孔成核；(c) 细胞内结冰是冰界面处电瞬变导致膜损伤的结果。实验数据不支持这些理论中的任何一个，但与以下假说一致：质膜在跨膜渗透压的临界梯度下受损，细胞内结冰是这种损伤的结果。该假说的一个推论是，可以使用数学模型来设计方案，以避免渗透压的损伤梯度，从而为通过快速冷却保存细胞、组织和器官提供新方法。
