Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/13224
Title: Hydrogen peroxide enhanced iron-induced injury in isolated heart and ventricular cardiomyocyte in rats
Authors: Chen, YY
Ho, KP
Xia, Q
Qian, ZM
Keywords: Cell-permeable iron (Fe-HQ)
Hydrogen peroxide
Isolated perfused rat heart
Isolated ventricular cardiomyocyte
Lactate dehydrogenase (LDH)
Creatine kinase (CK)
Malondialdehyde (MDA)
Left ventricular developed pressure (LVDP)
Issue Date: 2002
Publisher: Kluwer Academic Publ
Source: Molecular and cellular biochemistry, 2002, v. 231, no. 1-2, p. 61-68 How to cite?
Journal: Molecular and Cellular Biochemistry 
Abstract: To explore the cardiac effects of iron with or without hydrogen peroxide, the isolated perfused rat heart and enzymatically isolated ventricular cardiomyocyte were used. It was shown that treatment with cell-permeable iron (Fe-HQ) for 10 min reduced the contractile amplitude and velocity and end diastolic cell length in the cardiomyocyte and increased the contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary effluent and malondialdehyde (MDA) in the myocardium. The left ventricular developed pressure (LVDP), +/- dP/dtmax, and heart rate and coronary flow are showed a biphasic phase, an increase at first followed by a decline. Treatment with hydrogen peroxide for 10 min following Fe-HQ augmented the effect of iron with an increase in coronary LDH and CK release and myocardial MDA content, and decrease in LVDP, +/- dP/dtmax and heart rate. Perfusion of reduced glutathione with hydrogen peroxide counteracted these effects of Fe-HQ and hydrogen peroxide while dimethyl sulfoxide had no effect on the injury induced by Fe-HQ and hydrogen peroxide in the isolated rat heart. This suggests that augmentation of myocardial injury as a result of an increase in intracellular iron by hydrogen peroxide might involve the dysfunction of sulfydryl group containing proteins but not the hydroxyl radicals.
URI: http://hdl.handle.net/10397/13224
ISSN: 0300-8177
DOI: 10.1023/A:1014484907291
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