The protein kinase C inhibitor K252a, inhibits superoxide production in human neutrophils activated by both PIP2-dependent and -independent mechanisms

Abstract We report that the putative protein kinase C inhibitor, K252a, at concentrations of 0.2 and 1 μM, inhibited the respiratory burst induced by fluoride and formyl-methionyl-leucyl-phenyl-alanine respectively, both in human neutrophils primed with a subthreshold dose of phorbol myristate acetate and in non-primed neutrophils. In addition, K252a effectively inhibited ConA-zymosan-mediated superoxide generation in Ca 2+ -depleted neutrophils, with virtually maximal inhibition seen at 1 μM. These results suggest that protein kinase C is involved in the putative phosphalinositol bisphosphate-independent signal transduction mechanism of the respiratory burst as well as the pathway dependent on phosphatidylinositol bisphosphate hydrolysis.