The effect of the sulphur compound N-acetylcysteine (NAC) on certain receptor-mediated cellular functions [chemiluminescence (CL), phagocytosis and degranulation] in human neutrophils was studied, to evaluate how a scavenger of certain toxic oxygen product can protect the phagocyte and the bystander tissue cells from oxidative damage. When using IgG-opsonized yeast particles as stimulating agent, preincubating the neutrophils with NAC (0.25 mg/ml = 1.5 mM) increased both the CL response and phagocytosis. Higher concentrations of NAC (0.50-1.00 mg/ml = 3-6 mM) decreased the CL response, whereas the phagocytic capacity was still enhanced. This effect was more pronounced with adherent neutrophils than with neutrophils in suspension. No increased CL or phagocytic activity was, however, induced by NAC when C3bi-opsonized particles were used as a prey. From the fact that NAC (i) inhibited extracellularly localized myeloperoxidase dependent activities, and (ii) had no effect on neutrophils from patients with chronic granulomatous disease (CGD), we conclude that the scavenger effect of NAC not only reduces the accumulation of oxidative metabolites per se, but also enhances receptor-mediated phagocytosis by protecting Fc(IgG)-receptors from oxidative damage mediated by myeloperoxidase (MPO) and hydrogen peroxide (H2O2). Since NAC can increase phagocytosis and reduce the extracellularly produced oxidative metabolites, we furthermore conclude that NAC possesses some ideal properties as an anti-inflammatory agent.