Cittadini A, Dani A M, Wolf F, Bossi D, Calviello G
Biochim Biophys Acta. 1982 Mar 23;686(1):27-35. doi: 10.1016/0005-2736(82)90148-1.
Passive Ca2+ entry into Ehrlich ascites tumour cells has been investigated. Passive equilibrium of Ca2+ takes place in ascites tumour cells only under conditions of exhaustive energy depletion. The specific Ca2+ ionophore A23187 does not affect Ca2+ entry into ascites tumour cells under active metabolic conditions, but it increases the rate of Ca2+ equilibration in ascites tumour cells in the early stages of energy depletion. The results of the present experiments lead to the conclusion that in ascites tumour cell plasma membrane Ca2+ permeability is not a limiting step in the regulation of intracellular calcium content, while the energy-dependent Ca2+ extrusion is the main mechanism that prevents uncontrolled intracellular Ca2+ increase. The results taken together support the hypothesis that increased Ca2+ influx into the cell, caused by plasma membrane alteration, is responsible for permanently elevated mitotic activity and for deranged metabolic behavior of these neoplastic cells.
已对钙离子被动进入艾氏腹水瘤细胞的情况进行了研究。钙离子的被动平衡仅在能量彻底耗尽的条件下才会在腹水瘤细胞中发生。特定的钙离子载体A23187在活跃代谢条件下不会影响钙离子进入腹水瘤细胞,但在能量耗尽的早期阶段会提高腹水瘤细胞中钙离子平衡的速率。本实验结果得出结论,在腹水瘤细胞质膜中,钙离子通透性不是调节细胞内钙含量的限制步骤,而能量依赖性钙离子外排是防止细胞内钙离子不受控制增加的主要机制。综合这些结果支持了这样一种假说,即由质膜改变引起的细胞内钙离子流入增加,是这些肿瘤细胞有丝分裂活性持续升高和代谢行为紊乱的原因。