Abstract
Isolated human neutrophils produced no detectable (<10 nM) nitric oxide (NO) before or after activation with phorbol 12-myristate 13-acetate (PMA) or a chemotactic peptide, N-formyl- l-methionyl- l-leucyl- l-phenylalanine. Physiological levels of NO (1 μM) added before or after neutrophil activation had no effect on their respiratory burst oxygen consumption. Neutrophils activated with PMA caused very rapid breakdown of exogenously added NO. NO breakdown rates recorded at 250 nM NO were 0.09±0.02 and 3.77±0.23 nmol NO/min/10 6 cells ( n=3) before and after activation respectively and addition of copper-zinc superoxide dismutase during activation significantly decreased this rate (1.06±0.09 nmol NO/min/10 6 cells ( n=3)), suggesting that superoxide (O − 2) production was mainly responsible for the NO breakdown. These results suggest that activation of human neutrophils in vivo will dramatically decrease surrounding NO levels, potentially causing vasoconstriction, platelet aggregation and adhesion and peroxynitrite (ONOO −) formation.
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