Nitric oxide attenuates hydrogen peroxide-mediated injury to porcine pulmonary artery endothelial cells
Gupta, M.P.; Evanoff, V.; Hart, C.M.
American Journal of Physiology 272(6 Pt 1): L1133-L1141
1997
ISSN/ISBN: 0002-9513 PMID: 9227515 Document Number: 473601
To examine the role of nitric oxide ( cntdot NO) in vascular endothelial cell injury, cultured porcine pulmonary artery endothelial cells (PAEC) were treated with H-2O-2 (100-500 mu-M) for 30 min in the presence or absence of the cntdot NO donors (+-)S-nitroso-N-acetylpenicillamine (SNAP) or diethylamine nitric oxide (DEANO). H-2O-2 caused dose-dependent PAEC cytotoxicity detected 2 h after H-2O-2 treatment as the release of lactate dehydrogenase. SNAP (100 mu-M) and DEANO (100 mu-M) attenuated H-2O-2-induced cytotoxicity if present during H-2O-2 treatment. In contrast, restricting treatment with cntdot NO donors to periods before (30 min) or after (2 h) incubation with H-2O-2 did not prevent PAEC injury. Furthermore, the cntdot NO synthase inhibitor N-G-nitro-L-arginine methyl ester (1 mM) sensitized PAEC to H-2O-2-induced injury. SNAP also attenuated H-2O-2-induced PAEC lipid peroxidation even if restricted to periods before or after exposure to H-2O-2. Thus, although cntdot NO effectively attenuated H-2O-2-mediated PAEC lipid peroxidation and cytotoxicity, these effects were clearly dissociated, suggesting that the antiperoxidative effects of cntdot NO are not sufficient to account for its cytoprotective properties.