Coenzyme Q 10 and related quinones oxidize H 2 S to polysulfides and thiosulfate

In the canonical pathway for mitochondrial H S oxidation electrons are transferred from sulfide:quinone oxidoreductase (SQR) to complex III via ubiquinone (CoQ ). We previously observed that a number of quinones directly oxidize H S and we hypothesize that CoQ may have similar properties. Here we ex...

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Bibliographic Details
Published in:Free radical biology & medicine 2022-03, Vol.182, p.119
Main Authors: Olson, Kenneth R, Clear, Kasey J, Derry, Paul J, Gao, Yan, Ma, Zhilin, Wu, Gang, Kent, Thomas A, Straub, Karl D
Format: Article
Language:English
Subjects:
Hydrogen Sulfide - metabolism
Metal Nanoparticles
Oxidation-Reduction
Quinones
Silver
Sulfides - metabolism
Thiosulfates
Ubiquinone - metabolism
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Summary:In the canonical pathway for mitochondrial H S oxidation electrons are transferred from sulfide:quinone oxidoreductase (SQR) to complex III via ubiquinone (CoQ ). We previously observed that a number of quinones directly oxidize H S and we hypothesize that CoQ may have similar properties. Here we examine H S oxidation by CoQ and more hydrophilic, truncated forms, CoQ and CoQ , in buffer using H S and polysulfide fluorophores (AzMC and SSP4), silver nanoparticles to measure thiosulfate (H S O ), mass spectrometry to identify polysulfides and O -sensitive optodes to measure O consumption. We show that all three quinones concentration-dependently catalyze the oxidization of H S to polysulfides and thiosulfate in buffer with the potency CoQ >CoQ >CoQ and that CoQ specifically oxidizes H S to per-polysulfides, H S . These reactions consume and require oxygen and are augmented by addition of SOD suggesting that the quinones, not superoxide, oxidize H S. Related quinones, MitoQ, menadione and idebenone, oxidize H S in similar reactions. Exogenous CoQ decreases cellular H S and increases polysulfides and thiosulfate production and this is also O -dependent, suggesting that the quinone has similar effects on sulfur metabolism in cells. Collectively, these results suggest an additional endogenous mechanism for H S metabolism and a potential therapeutic approach in H S-related metabolic disorders.
ISSN:1873-4596