Effects of selected inhibitors on electron transport in Neisseria gonorrhoeae

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Abstract
The electron transport system of N. gonorrhoeae was partially characterized by using spectrophotometric, spectroscopic and O2 consumption measurements. The effects of selected electron transport inhibitors (amytal, rotenone, 2-heptyl-4-hydroxyquinoline, antimycin A1 and potassium cyanide [KCN]) on electron transfer in whole-cell and sonically treated whole-cell preparations of N. gonorrhoeae were examined. The oxidation of NADH, measured as a decrease in absorbance at 340 nm, was inhibited by each of the compounds tested. O2 consumption stimulated by NADH was also inhibited, whereas O2 uptake stimulated by succinate and malate was inhibited by KCN alone, suggesting the presence of a KCN-sensitive terminal oxidase. Room temperature optical difference spectra indicate an operational electron bypass around the amytalrotenone-binding site. Difference spectra in the presence of 2-heptyl-4-hydroxyquinoline suggest a possible site of interaction of this compound at the substrate side of cytochrome b. Reduced-minus-oxidized spectra of ascorbate-tetramethyl-p-phenylenediamine suggest the participation of b-, a- and d-type cytochromes in terminal oxidase activity. N. gonorrhoeae appears to have an electron transport chain containing cytochrome c, 2 b-type cytochromes (1 of which has an oxidase function), and possibly a- and d-type cytochromes. An abbreviated chain exists through which succinate and malate can be oxidized directly by a KCN-sensitive component.