Reactive oxygen species inhibit hyposmotic stress-dependent volume regulation in cultured rat cardiomyocytes.

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.

authors

Díaz-Elizondo J,Chiong M,Rojas-Rivera D,Olea-Azar C,Kwon HM,Lavandero S

doi

10.1016/j.bbrc.2006.10.004

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

1076-81

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)02229-7

journal_volume

350

pub_type

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