Medical Journals

Reactive Oxygen Species Inhibit Hyposmotic Stress-dependent Volume Regulation in Cultured Rat Cardiomyocytes.

Authors:
  • Díaz-Elizondo Jessica
  • Chiong Mario
  • Rojas-Rivera Diego
  • Olea-Azar Claudio
  • Kwon H Moo
  • Lavandero Sergio

From: Departamento Bioquímica y Biología Molecular, Universidad de Chile, Santiago 8380492, Chile.

Biochemical and biophysical research communications

  • Publish Date: Dec 2006
  • ISSN: 0006-291X
  • Volume: 350
  • Issue: 4
  • Pages: 1076-81
  • Medium: Print
  • Language: English
  • Citation (JAMA): Díaz-Elizondo Jessica, Chiong Mario, Rojas-Rivera Diego, et al. Reactive Oxygen Species Inhibit Hyposmotic Stress-dependent Volume Regulation in Cultured Rat Cardiomyocytes.. Biochem. Biophys. Res. Commun. Dec 2006;350:1076-81

Abstract

Cells have developed compensatory mechanisms to restore cell volume, and the ability to resist osmotic swelling or shrinkage parallels their resistance to necrosis or apoptosis. There are several mechanisms by which cells adapt to hyposmotic stress including that of regulatory volume decrease. In ischemia and reperfusion, cardiomyocytes are exposed to hyposmotic stress, but little is known as to how their volume is controlled. Exposure of cultured neonatal rat cardiomyocytes to hyposmotic media induced a rapid swelling without any compensatory regulatory volume decrease. The hyposmotic stress increased the production of reactive oxygen species, mainly through NADPH oxidase. Adenoviral overexpression of catalase inhibited the hyposmosis-dependent OH(*) production, induced the regulatory volume decrease mechanism, and prevented cell death. These results suggest that hyposmotic stress of cardiomyocytes stimulates production of reactive oxygen species which are closely linked to volume regulation and cell death.

Mesh Headings (Keywords): Animals, Animals, Newborn, Cell Size, Cells, Cultured, Myocytes, Cardiac, Osmotic Pressure, Oxidative Stress, Rats, Reactive Oxygen Species, Water-Electrolyte Balance


Check for Full Text / PubMed Unique Identifier (PMID): 17045960


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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