@article{0783f50954a046beb6c58e78f85f0ee2,
title = "Effects of hydrogen sulfide on mitochondrial function and cellular bioenergetics",
abstract = "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.",
keywords = "Bioenergetics, Cell signaling, Hydrogen sulfide, Mitochondria, Sulfhydration/persulfidation, Sulfide oxidation",
author = "Paul, {Bindu D.} and Snyder, {Solomon H.} and Khosrow Kashfi",
note = "Funding Information: KK: Supported in part by the National Institutes of Health [ R24 DA018055; R01GM123508 ] and the Professional Staff Congress-City University of New York (PSC-CUNY) [ TRADB-49-271 ]. This work was supported in part by US Public Health Service Grant DA044123 (to S.H.S), the American Heart Association (AHA)-Allen Initiative in Brain Health and Cognitive Impairment (to S.H.S and associates) and the Solve ME/CFS Initiative (SMCI) to BDP. Funding Information: KK: Supported in part by the National Institutes of Health [R24 DA018055; R01GM123508] and the Professional Staff Congress-City University of New York (PSC-CUNY) [TRADB-49-271]. This work was supported in part by US Public Health Service Grant DA044123 (to S.H.S), the American Heart Association (AHA)-Allen Initiative in Brain Health and Cognitive Impairment (to S.H.S and associates) and the Solve ME/CFS Initiative (SMCI) to BDP. Publisher Copyright: {\textcopyright} 2020",
year = "2021",
month = jan,
doi = "10.1016/j.redox.2020.101772",
language = "English (US)",
volume = "38",
journal = "Redox Biology",
issn = "2213-2317",
publisher = "Elsevier BV",
}