Use of the quinone antibiotic streptonigrin to explore the iron and oxygen metabolism of Neisseria gonorrhoeae. Mechanisms of antibiotic action and resistance

Abstract

Gonococci treated with the quinone antibiotic streptonigrin develop KCN insensitive respiration resulting in the formation of superoxide. Streptonigrin effects require iron suggesting that catalysis of hydroxyl radical is involved. We have found that extracellular iron appears to be more important than intracellular iron in these events. Highly streptonigrin resistant bacteria were isolated; these organisms demonstrated significant reduction in superoxide formation, and moderate reduction in total cellular iron. Iron transport mutants demonstrated superoxide fromation equivalent to the parent strain. Quinone antibiotics induce superoxide dismutase and catalase in E. coli, but this effect could not be demonstrated in gonococci. Our results suggest multiple possible mechanisms of streptonigrin resistance of N. gonorrhoeae including: failue to reduce the quinone; decreased intracellular iron, altered catalysis of hydroxyl radical at the cell surface.