Chernavskii D S, Polezhaev A A, Volkov E I
Cell Biophys. 1982 Jun-Sep;4(2-3):143-61. doi: 10.1007/BF02918310.
A mathematical model of the regulation of cell division is suggested. The model is based on the hypothesis that the process giving rhythm to cell division is located in the cell membrane: i.e., the process of free-radical oxidation of membrane lipids. Much depends on the physical state of the membrane. In the membrane, phase transitions take place because of the changes in lipid composition. These transitions differ in normal and tumor cells: in normal cells they are sharp and hysteretic owing to the presence of a framework (membrane skeleton) on the surface of the membrane, while in tumor cells the integrity of the surface is violated so that the transitions are smooth. This model makes it possible to explain differences in the regulation of normal and cancer cell proliferation. Within the limits of the model, such phenomena as density dependent inhibition of growth, reverse transformation, influence of cyclic AMP and ions of Ca2+ on the cell cycle, the actions of serum and of proteases on the cycle, and so on, are explained. A rational scheme for the appearance of the selective damage found in tumor cells is proposed.
提出了一种细胞分裂调控的数学模型。该模型基于这样一种假设，即赋予细胞分裂节律的过程位于细胞膜中：即膜脂的自由基氧化过程。这很大程度上取决于膜的物理状态。在膜中，由于脂质组成的变化会发生相变。这些相变在正常细胞和肿瘤细胞中有所不同：在正常细胞中，由于膜表面存在一个框架（膜骨架），相变是尖锐且滞后的，而在肿瘤细胞中，表面的完整性受到破坏，使得相变是平滑的。该模型能够解释正常细胞和癌细胞增殖调控的差异。在该模型的范围内，解释了诸如生长的密度依赖性抑制、逆向转化、环磷酸腺苷和钙离子对细胞周期的影响、血清和蛋白酶对细胞周期的作用等现象。提出了肿瘤细胞中发现的选择性损伤出现的合理机制。
