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Mitochondrial electron transport as a source for nitric oxide in the unicellular green alga Chlorella sorokiniana
Author(s) -
Tischner Rudolf,
Planchet Elisabeth,
Kaiser Werner M.
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.09.004
Subject(s) - salicylhydroxamic acid , chlorella sorokiniana , nitrite , antimycin a , alternative oxidase , nitrate reductase , biochemistry , nitric oxide , nitrite reductase , chemistry , nitrate , oxidase test , chlorella , electron transport chain , biology , enzyme , botany , algae , organic chemistry
Wild type (WT), and nitrate reductase (NR)‐ and nitrite‐reductase (NiR)‐deficient cells of Chlorella sorokiniana were used to characterize nitric oxide (NO) emission. The NO emission from nitrate‐grown WT cells was very low in air, increased slightly after addition of nitrite (200 μM), but strongly under anoxia. Importantly, even completely NR‐free mutants, as well as cells grown on tungstate, emitted NO when fed with nitrite under anoxia. Therefore, this NO production from nitrite was independent of NR and other molybdenum cofactor enzymes. Cyanide and inhibitors of mitochondrial complex III, myxothiazol or antimycin A, but not salicylhydroxamic acid (inhibitor of alternative oxidase) inhibited NO production by NR‐free cells. In contrast, NiR‐deficient cells growing on nitrate accumulated nitrite and emitted NO at very high equal rates in air and anoxia. This NO emission was 50% inhibited by salicylhydroxamic acid, indicating that in these cells the alternative oxidase pathway had been induced and reduced nitrite to NO.