Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

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Abstract
This study addresses the interactive role of nitric oxide (NO) and reactive oxygen intermediates (ROI) by direct quantitation of NO and superoxide (O2 –) in human neutrophil (PMN)-endothelial cell (EC) coculture during PMN-mediated EC injury. The results directly demonstrate an inverse correlation between NO and ROI levels in PMN-EC coculture, which significantly alters the PMN-EC adhesion and PMN-mediated EC killing. N-formyl-methionyl-leucyl-phenylalanine (fMLF)-stimulated PMN adhesion to cytokine-treated EC was decreased (>25%) in the presence of S-nitroso-N-penicillamine, a NO donor. NO also inhibited EC killing by stimulated PMN, suggesting its cytoprotective role. In addition, a significant decrease in NO levels was observed in the PMN-EC coculture compared with the EC cultured alone (422.45 ± 35.76 vs. 800.79 ±41.69 pmol). The reduced NO levels were restored by the addition of superoxide dismutase, a scavenger of O2 –, suggesting that PMN-derived O2 – is involved in the neutralization of NO in the coculture. The results indicate an inverse correlation between NO and O2 – in PMN-EC interactions and suggest the need for a critical balance between these two radicals in the regulation of PMN-mediated tissue injury. J. Leukoc. Biol. 64: 185–191; 1998.

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