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Title: | Eukaryotic and Prokaryotic Sources of Colonic Hydrogen Sulfide Synthesis |
Authors: | Flannigan, Kyle L. |
Advisor: | Wallace, John L. Huizinga, Jan Bercik, Premek |
Department: | Medical Sciences |
Keywords: | Inflammation;Mucosal Defense;Ulcer;Repair;Bacteria;Microbiota;Gastroenterology;Gastroenterology |
Publication Date: | Oct-2012 |
Abstract: | <p>Hydrogen sulfide (H<sub>2</sub>S) is an important modulator of many aspects of digestive function, both in health and disease. Colonic tissue H<sub>2</sub>S synthesis increases markedly during injury and inflammation and contributes to resolution. Some of the bacteria residing in the colon also produce H<sub>2</sub>S. The extent to which bacterial H<sub>2</sub>S synthesis contributes to what is measured as colonic H<sub>2</sub>S synthesis is not clear. When comparing conventional and germ-free mice we found no differences in colonic H<sub>2</sub>S synthesis. Furthermore, we found that colonic H<sub>2</sub>S synthesis is markedly increased when colonic tissue is inflamed, and, in proportion to the extent of inflammation, however fecal H<sub>2</sub>S synthesis does not change. Finally, rats fed a B vitamin-deficient diet for 6 weeks exhibited significantly diminished colonic H<sub>2</sub>S synthesis, but fecal H<sub>2</sub>S synthesis was not different from that of rats on the control diet. Our results demonstrate that H<sub>2</sub>S production by colonic bacteria does not contribute significantly to what we measure as colonic tissue H<sub>2</sub>S production.</p> <p>In another study, the contributions of three enzymatic pathways to colonic H<sub>2</sub>S synthesis were determined in tissues taken from healthy rats and rats with colitis.<strong> </strong>The ability of colonic tissue to inactivate H<sub>2</sub>S was also determined. The majority of increased H<sub>2</sub>S 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 H<sub>2</sub>S synthesis, and the extent of granulocyte infiltration into the tissue did not appear to be a significant determinant of the levels of H<sub>2</sub>S production. Inactivation of H<sub>2</sub>S 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 H<sub>2</sub>S synthesis. Together, the increased production and decreased inactivation of H<sub>2</sub>S may contribute to promoting resolution of inflammation and repair of damaged colonic tissue.</p> |
URI: | http://hdl.handle.net/11375/12656 |
Identifier: | opendissertations/7523 8584 3352895 |
Appears in Collections: | Open Access Dissertations and Theses |
Files in This Item:
File | Size | Format | |
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fulltext.pdf | 2.99 MB | Adobe PDF | View/Open |
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