Shrinkage-induced Activation of the Na + /H + Exchanger in Ehrlich Ascites Tumor Cells: Mechanisms Involved in the Activation and a Role for the Exchanger in Cell Volume Regulation

1996 ◽  
Vol 149 (2) ◽  
pp. 141-159 ◽  
Author(s):  
S.F. Pedersen ◽  
B. Kramhøft ◽  
N.K. Jørgensen ◽  
E.K. Hoffmann
Keyword(s):  
Cell Volume ◽  
Tumor Cells ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Ehrlich Ascites Tumor ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Ehrlich Ascites

ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl− channels in adherent Ehrlich Lettré and NIH3T3 cells

2009 ◽  
Vol 297 (1) ◽  
pp. C198-C206 ◽  
Author(s):  
Ian Henry Lambert ◽  
Thomas Kjær Klausen ◽  
Andreas Bergdahl ◽  
Charlotte Hougaard ◽  
Else Kay Hoffmann
Keyword(s):  
Cell Volume ◽  
Tumor Cells ◽  
Driving Force ◽  
Ehrlich Ascites Tumor ◽  
Adherent Cells ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Cell Shrinkage ◽  
Kcl Cotransport ◽  
Ehrlich Ascites

Addition of H2O2 (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 H2O2-induced cell shrinkage was unaffected by the presence of clofilium and clotrimazole, which blocks volume-sensitive and Ca2+-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 H2O2-induced cell shrinkage was impaired in the presence of the KCl cotransport inhibitor (dihydro-indenyl)oxyalkanoic acid (DIOA), following substitution of NO3− for Cl−, and when the driving force for KCl cotransport was omitted. It is suggested that H2O2 activates electroneutral KCl cotransport in Ehrlich ascites tumor cells and not K+ and Cl− channels. Addition of H2O2 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 H2O2 on cell volume was blocked by the serine-threonine phosphatase inhibitor calyculin A, indicating an important role of serine-threonine phosphorylation in the H2O2-mediated activation of KCl cotransport in Ehrlich cells. In contrast, addition of H2O2 to adherent cells, e.g., Ehrlich Lettré 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, H2O2 induces KCl cotransport or K+ and Cl− channels in nonadherent and adherent cells, respectively.

Mechanisms in Volume Regulation in Ehrlich Ascites Tumor Cells

1988 ◽  
Vol 11 (3-5) ◽  
pp. 221-247 ◽  
Author(s):  
Else K. Hoffmann ◽  
Ian Henry Lambert ◽  
Lars Ole Simonsen
Keyword(s):  
Tumor Cells ◽  
Volume Regulation ◽  
Ehrlich Ascites Tumor ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Ehrlich Ascites
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