| ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettré and NIH3T3 cells. | |
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MedLine Citation:
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PMID: 19419998 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Ian Henry Lambert; Thomas Kjaer Klausen; Andreas Bergdahl; Charlotte Hougaard; Else Kay Hoffmann |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2009-05-06 |
Journal Detail:
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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:
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Created Date: 2009-07-02 Completed Date: 2009-08-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C198-206 Citation Subset: IM |
Affiliation:
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Dept. of Biology, The August Krogh Building, Universitetsparken 13, DK-2100, Copenhagen Ø, Denmark. ihlambert@bio.ku.dk |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Carboxylic Acids / pharmacology Carcinoma, Ehrlich Tumor / metabolism* Cell Adhesion* Cell Line, Tumor Cell Size Chloride Channels / metabolism* Enzyme Inhibitors / pharmacology Female Fibroblasts / metabolism* Hydrogen Peroxide / metabolism Hypotonic Solutions Indenes / pharmacology Ion Transport Mice NIH 3T3 Cells Nitrates / metabolism Osmotic Pressure Oxazoles / pharmacology Oxidative Stress* Phosphoprotein Phosphatases / metabolism Phosphorylation Potassium Channels / metabolism* Reactive Oxygen Species / metabolism* Symporters / metabolism* Time Factors |
| Chemical | |
Reg. No./Substance:
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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 3.1.3.16/Phosphoprotein Phosphatases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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