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Hydrogen sulfide (H2S) is a malodorous and toxic gas. Nevertheless, recent evidence suggests that H2S is an endogenous mediator, joining nitric oxide and carbon monoxide as a third gaseous transmitter, and is increasingly being recognised as a key regulator of several cell processes and organ functions under both normal and pathological conditions.
H2S can be generated in mammalian tissues by a number of different processes. It can be enzymatically synthesised from cysteine by cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase in combination with cysteine aminotransferase. There are also inorganic sources of H2S such as the non-enzymatic haem-dependent reduction of sulfur. Also from a gut perspective, H2S can be generated by the colonic microbiota before diffusing from the lumen into the intestinal mucosa to reach subepithelial targets within the gut wall. However, counteracting the build up of endogenous H2S and potential toxic actions are protective mechanisms that degrade H2S, and this is especially true of the intestinal epithelium which is extremely efficient at reducing H2S to thiosulfate.1
Since the first description of a physiological function for H2S in enhancing N-methyl-d-aspartate (NMDA) receptor-mediated responses and facilitating the induction of long-term potentiation in the hippocampus,2 a host of effects have been reported in almost every cell or organ system studied to date.3–5 Inhibitors of CSE and CBS have been used to demonstrate a role for endogenous H2S, and its role as a physiological regulator of blood pressure is apparent in the CSE knockout mouse which develops hypertension.6 In the gastrointestinal (GI) tract H2S-synthesising enzymes have been shown to be expressed in the enteric nervous system,7 and H2S …
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