Azide‐stimulated oxygen consumption by the green alga Selenastrum minutum

Abstract

Dark O2 consumption by the green alga Selenastrum minutum was sensitive to inhibition by the cytochrome pathway respiration inhibitor cyanide in the absence of an alternative oxidase inhibitor, consistent with previous work that suggested that this alga lacks alternative oxidase capacity. In contrast, addition of low concentrations of the cytochrome pathway inhibitor azide (50–750 μM) resulted in a stimulation of dark O2 consumption, while higher concentrations of azide (1–2 mM) partially inhibited O2 consumption. Measurements of changes in cellular levels of pyruvate, malate and pyridine nucleotides upon cyanide addition were consistent with the absence of alternative oxidase capacity, and suggested that cyanide inhibition of O2 consumption was not due to nonspecific effects of cyanide. Addition of salicylhydroxamic acid (SHAM) also resulted in an increase in the rate of O2 consumption. Both azide‐ and SHAM‐stimulated O2 consumption were sensitive to inhibition by 50 mM ascorbate or by cyanide. However, the ubiquinone analogs chloroquine and quinacrine specifically inhibited azide‐stimulated O2 consumption, with only minor effects on SHAM‐stimulated O2 consumption. These results suggest that azide‐stimulated O2 consumption was not mediated by the previously characterized SHAM‐stimulated oxidase, and are consistent with the possibility that azide‐stimulated O2 consumption is mediated by a plasma membrane redox system.