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The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index.

Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part I. Biochemical and physiological mechanisms

Open access
Szabo, Csaba, Ransy, Céline, Módis, Katalin, Andriamihaja, Mireille, Murghes, Baptiste, Coletta, Ciro, Olah, Gabor, Yanagi, Kazunori, Bouillaud, Frédéric·2014·British Journal of Pharmacology
DOI 10.1111/bph.12369
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Abstract

Until recently, hydrogen sulfide (H 2 S) was exclusively viewed a toxic gas and an environmental hazard, with its toxicity primarily attributed to the inhibition of mitochondrial C omplex IV, resulting in a shutdown of mitochondrial electron transport and cellular ATP generation. Work over the last decade established multiple biological regulatory roles of H 2 S, as an endogenous gaseous transmitter. H 2 S is produced by cystathionine γ‐lyase (CSE), cystathionine β‐synthase (CBS) and 3‐mercaptopyruvate sulfurtransferase (3‐MST). In striking contrast to its inhibitory effect on C omplex IV, recent studies showed that at lower concentrations, H 2 S serves as a stimulator of electron transport in mammalian cells, by acting as a mitochondrial electron donor. Endogenous H 2 S, produced by mitochondrially localized 3‐MST, supports basal, physiological cellular bioenergetic functions; the activity of this metabolic support declines with physiological aging. In specialized conditions (calcium overload in vascular smooth muscle, colon cancer cells), CSE and CBS can also associate with the mitochondria; H 2 S produced by these enzymes, serves as an endogenous stimulator of cellular bioenergetics. The current article overviews the biochemical mechanisms underlying the stimulatory and inhibitory effects of H 2 S on mitochondrial function and cellular bioenergetics and discusses the implication of these processes for normal cellular physiology. The relevance of H 2 S biology is also discussed in the context of colonic epithelial cell physiology: colonocytes are exposed to high levels of sulfide produced by enteric bacteria, and serve as a metabolic barrier to limit their entry into the mammalian host, while, at the same time, utilizing it as a metabolic ‘fuel’. Linked Articles: This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue‐8

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Metadata

Authors
Szabo, C., Ransy, C., Módis, K., Andriamihaja, M., Murghes, B., Coletta, C., Olah, G., Yanagi, K., & Bouillaud, F.
Venue
British Journal of Pharmacology
Publisher
Wiley
Published
2014-03-28
Volume
171
Issue
8
Pages
2099-2122
ISSN
  • 0007-1188 (ISSN-L)
  • 1476-5381
DOI
10.1111/bph.12369
OpenAlex
W1655368476
Cited by
440
References
98
FWCI
10.05
Type
journal article
Language
en
Open access
hybrid

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