The influence of superoxide on the production of hypochlorous acid by human neutrophils

Abstract

Human neutrophils stimulated with opsonized zymosan 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 myeloperoxidase-dependent production of HOCl.