Nitric oxide reduces hydrogen peroxide production from human polymorphonuclear neutrophils.

Nitric oxide has been reported to affect both adhesion and respiratory burst of neutrophils. This indicates a possible role of nitric oxide in regulation of acute inflammatory responses. Release of oxygen metabolites from neutrophils can be measured using luminol-enhanced chemiluminescence and this method can detect both extracellularly and intracellularly released oxygen metabolites. Neutrophils treated with nitroprusside and activated with FMLP, type I collagen or PMA decreased their extracellular release of oxygen metabolites, while their intracellular release was almost unaffected. The effect of nitroprusside was mediated by nitric oxide since treatment with cyanide had the opposite effect. N-ethylmalemide treatment decreased both extra- and intracellular release of oxygen metabolites. This indicates that nitric oxide affects membrane-bound NADPH-oxidase either indirectly or directly, and not a cytosol factor of the oxidase as earlier shown for N-ethylmaleimide. In conclusion, extracellular nitric oxide attenuates extracellularly released oxygen metabolites from activated neutrophils in an inflammatory response.