Complexities of complex II: Sulfide metabolism in vivo

J Biol Chem. 2022 Mar;298(3):101661. doi: 10.1016/j.jbc.2022.101661. Epub 2022 Jan 29.

Abstract

High levels of H2S produced by gut microbiota can block oxygen utilization by inhibiting mitochondrial complex IV. Kumar et al. have shown how cells respond to this inhibition by using the mitochondrial sulfide oxidation pathway and reverse electron transport. The reverse activity of mitochondrial complex II (succinate-quinone oxidoreductase, i.e., fumarate reduction) generates oxidized coenzyme Q, which is then reduced by the mitochondrial sulfide quinone oxidoreductase to oxidize H2S. This newly identified redox circuitry points to the importance of complex II reversal in mitochondria during periods of hypoxia and cellular stress.

Keywords: coenzyme Q; complex II; electron transport; fumarate reductase; hydrogen sulfide; hypoxia; mitochondria; succinate dehydrogenase; sulfide quinone oxidoreductase.

Publication types

  • Comment

MeSH terms

  • Electron Transport
  • Electron Transport Complex II* / metabolism
  • Electron Transport Complex IV / antagonists & inhibitors
  • Electron Transport Complex IV / metabolism
  • Hydrogen Sulfide* / metabolism
  • Oxidation-Reduction
  • Sulfides* / metabolism

Substances

  • Sulfides
  • Electron Transport Complex II
  • Electron Transport Complex IV
  • Hydrogen Sulfide