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Am J Physiol Cell Physiol 274: C245-C252, 1998;
0363-6143/98 $5.00
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Vol. 274, Issue 1, C245-C252, January 1998

Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes

Junsuke Igarashi1,2, Masashi Nishida1,2, Shiro Hoshida2, Nobushige Yamashita2, Hiroaki Kosaka3, Masatsugu Hori2, Tsunehiko Kuzuya1,2, and Michihiko Tada1,2

1 The Department of Pathophysiology, 2 The First Department of Medicine, and 3 The First Department of Physiology, Osaka University Medical School, Suita, Osaka 565, Japan

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined. Interleukin-1beta induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS, L-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso-N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2 (0.1 mM, 1 h). Inhibition of iNOS with Nomega -nitro-L-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

heart; interleukin-1beta ; glutathione peroxidase; antisense oligodeoxyribonucleotide


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