35
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Hydrogen Sulfide in Physiology and Diseases of the Digestive Tract

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Hydrogen sulfide (H 2S) is a Janus-faced molecule. On one hand, several toxic functions have been attributed to H 2S and exposure to high levels of this gas is extremely hazardous to health. On the other hand, H 2S delivery based clinical therapies are being developed to combat inflammation, visceral pain, oxidative stress related tissue injury, thrombosis and cancer. Since its discovery, H 2S has been found to have pleiotropic effects on physiology and health. H 2S is a gasotransmitter that exerts its effect on different systems, such as gastrointestinal, neuronal, cardiovascular, respiratory, renal, and hepatic systems. In the gastrointestinal tract, in addition to H 2S production by mammalian cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), H 2S is also generated by the metabolic activity of resident gut microbes, mainly by colonic Sulfate-Reducing Bacteria (SRB) via a dissimilatory sulfate reduction (DSR) pathway. In the gut, H 2S regulates functions such as inflammation, ischemia/ reperfusion injury and motility. H 2S derived from gut microbes has been found to be associated with gastrointestinal disorders such as ulcerative colitis, Crohn’s disease and irritable bowel syndrome. This underscores the importance of gut microbes and their production of H 2S on host physiology and pathophysiology.

          Related collections

          Most cited references141

          • Record: found
          • Abstract: found
          • Article: not found

          Gut inflammation provides a respiratory electron acceptor for Salmonella

          Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through unknown mechanisms. Here we show that reactive oxygen species generated during inflammation reacted with endogenous, luminal sulphur compounds (thiosulfate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to utilize tetrathionate as an electron acceptor produced a growth advantage for S. Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use respiration to compete with fermenting gut microbes. Thus, the ability to trigger intestinal inflammation is crucial for the biology of this diarrhoeal pathogen.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            H2S signals through protein S-sulfhydration.

            Hydrogen sulfide (H2S), a messenger molecule generated by cystathionine gamma-lyase, acts as a physiologic vasorelaxant. Mechanisms whereby H2S signals have been elusive. We now show that H2S physiologically modifies cysteines in a large number of proteins by S-sulfhydration. About 10 to 25% of many liver proteins, including actin, tubulin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), are sulfhydrated under physiological conditions. Sulfhydration augments GAPDH activity and enhances actin polymerization. Sulfhydration thus appears to be a physiologic posttranslational modification for proteins.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The possible role of hydrogen sulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide.

              Hydrogen sulfide (H2S), which is well known as a toxic gas, is produced endogenously in mammalian tissues from L-cysteine mainly by two pyridoxal-5'-phosphate-dependent enzymes, cystathionine beta-synthetase and cystathionine gamma-lyase. Recently, we showed that cystathionine beta-synthetase in the brain produces H2S, and that H2S facilitates the induction of hippocampal long-term potentiation by enhancing NMDA receptor activity. Here we show that mRNA for another H2S producing enzyme, cystathionine gamma-lyase, is expressed in the ileum, portal vein, and thoracic aorta. The ileum also expresses cystathionine beta-synthetase mRNA. These tissues produce H2S, and this production is blocked by cystathionine beta-synthetase and cystathionine gamma-lyase specific inhibitors. Although exogenously applied H2S alone relaxed these smooth muscles, much lower concentrations of H2S greatly enhanced the smooth muscle relaxation induced by NO in the thoracic aorta. These observations suggest that the endogenous H2S may regulate smooth muscle tone in synergy with NO.
                Bookmark

                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Microorganisms
                Microorganisms
                microorganisms
                Microorganisms
                MDPI
                2076-2607
                12 November 2015
                December 2015
                : 3
                : 4
                : 866-889
                Affiliations
                [1 ]Section of Gastroenterology, Medicine Service, New Mexico VA Health Care System, Albuquerque, NM 87108, USA; E-Mail: sbsingh14@ 123456salud.unm.edu
                [2 ]Division of Gastroenterology and Hepatology, Department of Medicine, the University of New Mexico, Albuquerque, NM 87131, USA
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: helin@ 123456salud.unm.edu ; Tel.: +1-505-265-1711 (ext. 4511, 4552).
                Article
                microorganisms-03-00866
                10.3390/microorganisms3040866
                5023273
                27682122
                1b7ce5c8-146e-410d-b05a-e01626972dea
                © 2015 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 01 September 2015
                : 04 November 2015
                Categories
                Review

                hydrogen sulfide,gastrointestinal tract,inflammation,ischemia/reperfusion injury,motility,sulfate reducing bacteria,desulfovibrio

                Comments

                Comment on this article