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Abstract
Human neutrophils stimulated with opsonized zyrnosan promoted hypochlorous acid (HOCl)-dependent loss of monochlorodimedon. Formation of HOCl was completely inhibited by catalase, and it was also inhibited up to 70% by SOD. There was no inhibition by desferal, DTPA, mannitol or dimethylsulphoxide. which excluded the involvement of -OH. Our results indicate that generation of O2-by neutrophils enables these cells to enhance their production of HOCl. Furthermore, inhibition of neutrophil processes by SOD and catalase does not necessarily implicate -OH. We propose that O2-may potentiate oxidant damage at inflammatory sites by boosting the rnyeloperoxidase-dependent production of HOCl