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Azide‐stimulated oxygen consumption by the green alga Selenastrum minutum
Author(s) -
Lynnes Jaret A.,
Weger Harold G.
Publication year - 1996
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.1996.tb00489.x
Subject(s) - salicylhydroxamic acid , cyanide , azide , cytochrome c oxidase , alternative oxidase , biochemistry , chemistry , respiration , oxidase test , biology , enzyme , botany , organic chemistry
Dark O 2 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 μ M ) resulted in a stimulation of dark O 2 consumption, while higher concentrations of azide (1–2 m M ) partially inhibited O 2 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 O 2 consumption was not due to nonspecific effects of cyanide. Addition of salicylhydroxamic acid (SHAM) also resulted in an increase in the rate of O 2 consumption. Both azide‐ and SHAM‐stimulated O 2 consumption were sensitive to inhibition by 50 m M ascorbate or by cyanide. However, the ubiquinone analogs chloroquine and quinacrine specifically inhibited azide‐stimulated O 2 consumption, with only minor effects on SHAM‐stimulated O 2 consumption. These results suggest that azide‐stimulated O 2 consumption was not mediated by the previously characterized SHAM‐stimulated oxidase, and are consistent with the possibility that azide‐stimulated O 2 consumption is mediated by a plasma membrane redox system.