Document Detail

ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettré and NIH3T3 cells.
MedLine Citation:
PMID:  19419998     Owner:  NLM     Status:  MEDLINE    
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 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, H(2)O(2) induces KCl cotransport or K(+) and Cl(-) channels in nonadherent and adherent cells, respectively.
Ian Henry Lambert; Thomas Kjaer Klausen; Andreas Bergdahl; Charlotte Hougaard; Else Kay Hoffmann
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-06
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  297     ISSN:  1522-1563     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-02     Completed Date:  2009-08-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C198-206     Citation Subset:  IM    
Dept. of Biology, The August Krogh Building, Universitetsparken 13, DK-2100, Copenhagen Ø, Denmark.
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MeSH Terms
Carboxylic Acids / pharmacology
Carcinoma, Ehrlich Tumor / metabolism*
Cell Adhesion*
Cell Line, Tumor
Cell Size
Chloride Channels / metabolism*
Enzyme Inhibitors / pharmacology
Fibroblasts / metabolism*
Hydrogen Peroxide / metabolism
Hypotonic Solutions
Indenes / pharmacology
Ion Transport
NIH 3T3 Cells
Nitrates / metabolism
Osmotic Pressure
Oxazoles / pharmacology
Oxidative Stress*
Phosphoprotein Phosphatases / metabolism
Potassium Channels / metabolism*
Reactive Oxygen Species / metabolism*
Symporters / metabolism*
Time Factors
Reg. No./Substance:
0/((dihydroindenyl)oxy)alkanoic acid; 0/Carboxylic Acids; 0/Chloride Channels; 0/Enzyme Inhibitors; 0/Hypotonic Solutions; 0/Indenes; 0/Nitrates; 0/Oxazoles; 0/Potassium Channels; 0/Reactive Oxygen Species; 0/Symporters; 0/potassium-chloride symporters; 101932-71-2/calyculin A; 7722-84-1/Hydrogen Peroxide; EC Phosphatases

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