Eukaryotic and Prokaryotic Sources of Colonic Hydrogen Sulfide Synthesis

Abstract

<p>Hydrogen sulfide (H₂S) is an important modulator of many aspects of digestive function, both in health and disease. Colonic tissue H₂S synthesis increases markedly during injury and inflammation and contributes to resolution. Some of the bacteria residing in the colon also produce H₂S. The extent to which bacterial H₂S synthesis contributes to what is measured as colonic H₂S synthesis is not clear. When comparing conventional and germ-free mice we found no differences in colonic H₂S synthesis. Furthermore, we found that colonic H₂S synthesis is markedly increased when colonic tissue is inflamed, and, in proportion to the extent of inflammation, however fecal H₂S synthesis does not change. Finally, rats fed a B vitamin-deficient diet for 6 weeks exhibited significantly diminished colonic H₂S synthesis, but fecal H₂S synthesis was not different from that of rats on the control diet. Our results demonstrate that H₂S production by colonic bacteria does not contribute significantly to what we measure as colonic tissue H₂S production.</p> <p>In another study, the contributions of three enzymatic pathways to colonic H₂S synthesis were determined in tissues taken from healthy rats and rats with colitis.<strong> </strong>The ability of colonic tissue to inactivate H₂S was also determined. The majority of increased H₂S synthesis, in both healthy and inflamed tissue, was derived via a pyroxidal-5’-phosphate-independent pathway. Ulcerated mucosal tissue accounted for the greatest levels of H₂S synthesis, and the extent of granulocyte infiltration into the tissue did not appear to be a significant determinant of the levels of H₂S production. Inactivation of H₂S by colonic tissue occurred rapidly, but was significantly reduced in ulcerated colonic tissue from rats with colitis. Damage to colonic tissue appears to be the major stimulus for enhanced H₂S synthesis. Together, the increased production and decreased inactivation of H₂S may contribute to promoting resolution of inflammation and repair of damaged colonic tissue.</p>