Regulatory volume increase in Ehrlich ascites tumor cells.
Regulatory volume increase in Ehrlich ascites tumor cells.
复制标题
艾利希腹水肿瘤细胞的调节体积增加。
DOI：
10.1016/0005-2736(90)90375-x
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Levinson,C
中科院分区：
文献类型：
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作者：
Levinson,C
艾利希腹水肿瘤细胞因 KCl 耗尽和 Na+ 负载而缩小，通过 Na+/K+ 泵和 (2Cl−+ K++ Na+) 共转运系统的联合活性重新建立正常离子浓度。然而，细胞体积的恢复仅与细胞内 Cl− 的增加相关。这与平衡体积与稳态 [Cl−] 线性相关的发现一起表明，细胞体积增加的程度是由 Cl− 运输决定的。净 Cl− 吸收几乎完全由共转运系统介导，最终负责建立稳态细胞内 Cl− 浓度。当 Na+、K+ 和 Cl− 的化学势之和接近零时，该途径介导的运输停止，并且对应于 Cl− 稳态的建立。这些发现表明 Cl−。这些发现表明 Cl− 在净协同转运活性以及细胞体积的调节中发挥着关键作用。
Ehrlich ascites tumor cells, shrunken as a result of KCl-depletion and Na+loading, re-establish normal ionic concentrations by the combined activity of the Na+/K+pump and the (2Cl−+ K++ Na+) cotransport system. Restoration of cell volume, however, correlates only with the increase in intracellular Cl−. This along with the finding that the equilibrium volume is linearly related to the steady state [Cl−] suggests that the extent to which cell volume increases is determined by Cl−transport. Net Cl−uptake, which is mediated almost exclusively by the cotransport system, is ultimately responsible for establishing the steady-state intracellular Cl−concentration. Transport mediated by this pathway ceases when the sum of the chemical potentials for Na+, K+and Cl−approaches zero and corresponds with the establishment of a steady state for Cl−. These findings suggest that Cl−. These findings suggest that Cl−plays a key role in the regulation of net cotransport activity and thereby cell volume.