Journal
REDOX BIOLOGY
Volume 38, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.redox.2020.101772
Keywords
Mitochondria; Hydrogen sulfide; Sulfide oxidation; Bioenergetics; Cell signaling; Sulfhydration/persulfidation
Categories
Funding
- National Institutes of Health [R24 DA018055, R01GM123508]
- Professional Staff Congress-City University of New York (PSC-CUNY) [TRADB-49-271]
- US Public Health Service [DA044123]
- American Heart Association (AHA)-Allen Initiative in Brain Health and Cognitive Impairment
- Solve ME/CFS Initiative (SMCI)
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Hydrogen sulfide (H2S) was once thought to be only toxic, but is now known to also act as an endogenous signaling molecule. The effects of H2S on cellular physiology are dose-dependent, with lower concentrations being beneficial and higher concentrations being cytotoxic. In particular, H2S has contrasting effects on mitochondrial function, inhibiting the electron transport chain at higher concentrations and stimulating bioenergetics at lower concentrations.
Hydrogen sulfide (H2S) was once considered to have only toxic properties, until it was discovered to be an endogenous signaling molecule. The effects of H2S are dose dependent, with lower concentrations being beneficial and higher concentrations, cytotoxic. This scenario is especially true for the effects of H2S on mitochondrial function, where higher concentrations of the gasotransmitter inhibit the electron transport chain, and lower concentrations stimulate bioenergetics in multiple ways. Here we review the role of H2S in mitochondrial function and its effects on cellular physiology.
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