• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.75-85
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• 1989

In opsonized zymosan activated PMN leukocytes, N-ethylamleiamide and $Hg^{++}$, penetrable sulfhydryl group inhibitors, inhibited superoxide generation, NADPH oxidase activity and lysosomal enzyme (lactic dehydrogenase and ${\beta}-glucuronidase$) secretion. P-Chloromercuribenzoic acid and p-chloromercuribenzenesulfonic acid, surface sulfhydryl group inhibitors did not affect superoxide generation but effectively inhibited both NADPH oxidase activity and lysosomal enzyme secretion. During phagocytosis, contents of surface and soluble sulfhydryl groups were gradually decreased with increasing incubation times. N-ethylmaleiamide and $Hg^{++}$ caused a loss of both surface and soluble sulfhydryl groups. P-Chloromercuribenzoic acid and p-chloromercuribenzenesulfonic acid significantly decreased the surface sulfhydryl content but did not after soluble sulfhydryl groups. Cysteine and mercaptopropionylglycine inhibited superoxide generation and lysosomal enzyme secretion. Glutathione had no effect on superoxide generation but remarkably inhibited lactic dehydrogenase release. Suppression of superoxide generation by N-ethylmaleiamide was reversed by cysteine and mercaptopropionyl-glycine but not by glutathione. Inactivation of NADPH oxidase by N-ethylmaleiamide was prevented by glutathione, cysteine or mercaptopropionylglycine. Stimulated superoxide generaion by carbachol was completely abolished by N-ethylrnaleiamide and antagonized by atropine. Thus, the expression of PMN leukocyte response to external stimuli may be associated with the change of sulfhydryl groups content. It is suggested that lysosomal enzyme secretion is influenced by both surface and soluble sulfhydryl groups, whereas superoxide generation by intracellular soluble sulfhydryl groups.