Hydrogen sulfide (HS) has emerged as a critical mediator of multiple physiological processes in mammalian systems. The pathways involved in the production, consumption, and mechanism of action of HS appear to be sensitive to alterations in the cellular redox state and O tension. Indeed, the catabolism of HS through a putative oxidation pathway, the sulfide quinone oxido-reductase system, is highly dependent on O tension. Dysregulation of HS homeostasis has also been implicated in numerous pathological conditions and diseases. In this review, the chemistry and the main physiological actions of HS are presented. Some examples highlighting the cytoprotective actions of HS within the context of cardiovascular disease are also reported. Elucidation of the redox biology of HS will enable the development of new pharmacological agents based on this intriguing new redox cellular signal.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3685875 | PMC |
http://dx.doi.org/10.1016/j.redox.2012.11.006 | DOI Listing |
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