The role of surface sulphydryl (-SH) groups of human polymorphonuclear leucocytes on phagocytosis-associated oxidative metabolic changes was studied. p-Chloromercurybenzene sulphonic acid, a surface -SH group inhibitor, had no effect on phagocytosis, superoxide production during phagocytosis, or killing of S. aureus by the leucocytes, while it inhibited phagocytosis-associated stimulation of hexose monophosphate pathway activity and H2O2 production. In contrast, N-ethylmaleimide, which inhibits both intracellular and surface -SH groups, inhibited phagocytosis-associated oxidative metabolic changes. p-Chloromercurybenzene sulphonic acid also inhibited the stimulation of hexose monophosphate pathway activity by exogenous H2O2, suggesting a regulatory role of plasma membrane on the pathway's activity in human polymorphonuclear leucocytes. The results also suggest that: (I) superoxide production is the primary event of oxidative metabolic changes during phagocytosis, (2) superoxide plays an important role in the killing of S. aureus, and (3) the hexose monophosphate pathway plays a primary role in producing NADPH for H2O2 production from superoxide.
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