Oxidative injury of isolated cardiomyocytes: Dependence on free radical species

Citation
I. Durot et al., Oxidative injury of isolated cardiomyocytes: Dependence on free radical species, FREE RAD B, 29(9), 2000, pp. 846-857
Citations number
58
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
29
Issue
9
Year of publication
2000
Pages
846 - 857
Database
ISI
SICI code
0891-5849(20001101)29:9<846:OIOICD>2.0.ZU;2-F
Abstract
The contribution of lipid peroxidation to myocardial injury by free radical s (ER is still unclear. Consequently, we examined the functional damages in flicted on cultured rat cardiomyocytes (CM) during FR stress provoked by th e xanthine/xanthine oxidase system (X/XO) or by a hydroperoxidized fatty ac id ((9 Z, 11 E, 13 (S), 15 Z)-13-hydroperoxyocta-decatrienoic acid; 13-HpOT rE), in order to simulate in vitro the initial phase and the propagation ph ase of the FR attack, respectively. Transmembrane potentials were recorded with glass microelectrodes and contractions were monitored photometrically. The EPR spectroscopy showed that X/XO produced superoxide and hydroxyl rad icals during 10 min. The X/XO system altered sharply and irreversibly the s pontaneous electrical and mechanical activities of the CM. However, the gas chromatographic analysis showed that these drastic functional damages were associated with comparatively moderate membrane PUFA degradation Moreover, the EPR analysis did not reveal the production of lipid-derived FR. 13-HpO TrE induced a moderate and reversible decrease in electrical parameters, wi th no change in CM contractions. These results indicate that the functional consequences of FR attack are dependent on the radical species present and do not support the idea that the membrane lipid breakdown is a major facto r of myocardial oxidant dysfunction. (C) 2000 Elsevier Science Inc.