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http://hdl.handle.net/11375/12656
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DC Field | Value | Language |
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dc.contributor.advisor | Wallace, John L. | en_US |
dc.contributor.advisor | Huizinga, Jan | en_US |
dc.contributor.advisor | Bercik, Premek | en_US |
dc.contributor.author | Flannigan, Kyle L. | en_US |
dc.date.accessioned | 2014-06-18T17:00:18Z | - |
dc.date.available | 2014-06-18T17:00:18Z | - |
dc.date.created | 2012-09-27 | en_US |
dc.date.issued | 2012-10 | en_US |
dc.identifier.other | opendissertations/7523 | en_US |
dc.identifier.other | 8584 | en_US |
dc.identifier.other | 3352895 | en_US |
dc.identifier.uri | http://hdl.handle.net/11375/12656 | - |
dc.description.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> | en_US |
dc.subject | Inflammation | en_US |
dc.subject | Mucosal Defense | en_US |
dc.subject | Ulcer | en_US |
dc.subject | Repair | en_US |
dc.subject | Bacteria | en_US |
dc.subject | Microbiota | en_US |
dc.subject | Gastroenterology | en_US |
dc.subject | Gastroenterology | en_US |
dc.title | Eukaryotic and Prokaryotic Sources of Colonic Hydrogen Sulfide Synthesis | en_US |
dc.type | thesis | en_US |
dc.contributor.department | Medical Sciences | en_US |
dc.description.degree | Master of Science (MSc) | en_US |
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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