Reactive oxygen species inhibit hyposmotic stress-dependent volume regulation in cultured rat cardiomyocytes.
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.
Díaz-Elizondo
Jessica
J
Departamento Bioquímica y Biología Molecular, Universidad de Chile, Santiago 8380492, Chile.
Chiong
Mario
M
Rojas-Rivera
Diego
D
Olea-Azar
Claudio
C
Kwon
H Moo
HM
Lavandero
Sergio
S
D000818:Animals; D000831:Animals, Newborn; D048429:Cell Size; D002478:Cells, Cultured; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000502:physiology*; D009997:Osmotic Pressure; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology*
D017382:Reactive Oxygen Species