• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettre and NIH3T3 cells.
【24h】

ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettre and NIH3T3 cells.

机译：ROS激活非粘附性Ehrlich腹水细胞中的KCl共转运，但粘附Ehrlich Lettre和NIH3T3细胞中的K +和Cl-通道。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Addition of H(2)O(2) (0.5 mM) to Ehrlich ascites tumor cells under isotonic conditions results in a substantial (22 +/- 1%) reduction in cell volume within 25 min. The cell shrinkage is paralleled by net loss of K(+), which was significant within 8 min, whereas no concomitant increase in the K(+) or Cl(-) conductances could be observed. The H(2)O(2)-induced cell shrinkage was unaffected by the presence of clofilium and clotrimazole, which blocks volume-sensitive and Ca(2+)-activated K(+) channels, respectively, and is unaffected by a raise in extracellular K(+) concentration to a value that eliminates the electrochemical driving force for K(+). On the other hand, the H(2)O(2)-induced cell shrinkage was impaired in the presence of the KCl cotransport inhibitor (dihydro-indenyl)oxyalkanoic acid (DIOA), following substitution of NO(3)(-) for Cl(-), and when the driving force for KCl cotransport was omitted. It is suggested that H(2)O(2) activates electroneutral KCl cotransport in Ehrlich ascites tumor cells and not K(+) and Cl(-) channels. Addition of H(2)O(2) to hypotonically exposed cells accelerates the regulatory volume decrease and the concomitant net loss of K(+), whereas no additional increase in the K(+) and Cl(-) conductance was observed. The effect of H(2)O(2) on cell volume was blocked by the serine-threonine phosphatase inhibitor calyculin A, indicating an important role of serine-threonine phosphorylation in the H(2)O(2)-mediated activation of KCl cotransport in Ehrlich cells. In contrast, addition of H(2)O(2) to adherent cells, e.g., Ehrlich Lettre ascites cells, a subtype of the Ehrlich ascites tumor cells, and NIH3T3 mouse fibroblasts increased the K(+) and Cl(-) conductances after hypotonic cell swelling. Hence, H(2)O(2) induces KCl cotransport or K(+) and Cl(-) channels in nonadherent and adherent cells, respectively.
机译：在等渗条件下将H（2）O（2）（0.5 mM）添加到Ehrlich腹水肿瘤细胞导致细胞体积在25分钟内大幅减少（22 +/- 1％）。细胞收缩与K（+）的净损失平行，这在8分钟内是显着的，而没有观察到K（+）或Cl（-）电导的伴随增加。 H（2）O（2）诱导的细胞收缩不受Clofilium和clotrimazole的存在的影响，它们分别阻止体积敏感和Ca（2+）激活的K（+）通道，并且不受升高的影响胞外K（+）的浓度达到消除K（+）的电化学驱动力的值。另一方面，在KCl共转运抑制剂（二氢茚基）氧基链烷酸（DIOA）的存在下，用NO（3）（-）取代后，H（2）O（2）诱导的细胞收缩受到损害。 Cl（-），以及省略了KCl共运的驱动力。建议H（2）O（2）激活Ehrlich腹水肿瘤细胞而不是K（+）和Cl（-）通道的电中性KCl共转运。将H（2）O（2）添加到低渗暴露的细胞中会加速调节体积的减小和随之而来的K（+）的净损失，而未观察到K（+）和Cl（-）电导的额外增加。 H（2）O（2）对细胞体积的影响被丝氨酸-苏氨酸磷酸酶抑制剂calyculin A阻止，表明丝氨酸-苏氨酸磷酸化在H（2）O（2）介导的KCl激活中的重要作用在艾氏细胞中共转运。相反，将H（2）O（2）添加至贴壁细胞，例如Ehrlich Lettre腹水细胞，Ehrlich腹水肿瘤细胞的一种亚型和NIH3T3小鼠成纤维细胞后，K（+）和Cl（-）电导率增加。低渗细胞肿胀。因此，H（2）O（2）分别在非贴壁细胞和贴壁细胞中诱导KCl共转运或K（+）和Cl（-）通道。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号