Inability of Ehrlich ascites tumor cells to volume regulate following a hyperosmotic challenge.
Inability of Ehrlich ascites tumor cells to volume regulate following a hyperosmotic challenge.
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艾利希腹水肿瘤细胞在高渗挑战后无法调节体积。
DOI：
10.1007/bf01951561
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Levinson,C
中科院分区：
文献类型：
--
作者：
Levinson,C
当悬浮培养基的渗透压增加时，埃利希细胞收缩，并且至少在最初表现为渗透压计。随后的行为取决于高渗溶质的性质，但在任何情况下，细胞都没有表现出调节性体积增加。与高渗NaCl的渗透压响应，发现和所得的体积保持相对恒定。然而，在蔗糖诱导的高渗状态下观察到连续收缩。在这两种情况下，增加渗透压从300到500 mOsminitated细胞电解质含量的显着变化，以及细胞内pH值。这是由激活的Na+/H+交换，Na/K泵，Na+K +2Cl ~+共转运蛋白和损失的K+通过Ba-敏感的途径。协同转运蛋白对[Cl−]i升高（<100 mm）和/或Na+、K+和Cl−化学势向外梯度的增加作出反应，介导离子的净损失，这是含蔗糖培养基中细胞收缩的原因。然而，在高渗NaCl中，净Cl−通量几乎为零，表明最小的净共转运activity.We的结论，体积稳定性细胞收缩后依赖于跨膜梯度的化学势[Na++K++Cl−]，以及内到胞外[Cl−]的比例。这两个因素似乎影响的活动的共转运途径。
Ehrlich cells shrink when the osmolality of the suspending medium is increased and behave, at least initially, as osmometers. Subsequent behavior depends on the nature of the hyperosmotic solute but in no case did the cells exhibit regulatory volume increase. With hyperosmotic NaCl an osmometric response was found and the resultant volume maintained relatively constant. Continuous shrinkage was observed, however, with sucrose-induced hyperosmolality. In both cases increasing osmolality from 300 to 500 mOsminitiated significant changes in cellular electrolyte content, as well as intracellular pH. This was brought about by activation of the Na+/H+exchanger, the Na/K pump, the Na++K++2Cl−cotransporter and by loss of K+via a Ba-sensitive pathway. The cotransporter in response to elevated [Cl−]i(∼100mm) and/or the increase in the outwardly directed gradient of chemical potential for Na+, K+and Cl−, mediated net loss of ions which accounted for cell shrinkage in the sucrose-containing medium. In hyperosmotic NaCl, however, the net Cl−flux was almost zero suggesting minimal net cotransport activity.We conclude that volume stability following cell shrinkage depends on the transmembrane gradient of chemical potential for [Na++K++Cl−], as well as the ratio of intra- to extracellular [Cl−]. Both factors appear to influence the activity of the cotransport pathway.