Colonic Luminal Hydrogen Sulfide Is Not Elevated in Ulcerative Colitis

@article{Moore2004ColonicLH,
  title={Colonic Luminal Hydrogen Sulfide Is Not Elevated in Ulcerative Colitis},
  author={J. Moore and Wendy J Babidge and Susan Millard and William E W Roediger},
  journal={Digestive Diseases and Sciences},
  year={2004},
  volume={43},
  pages={162-165}
}
It has been proposed that the reduction inn-butyrate oxidation by colonic epithelial cellsobserved in ulcerative colitis may be related toexposure to reduced forms of sulfur derived fromdissimilatory sulfate reduction by luminal microflora. Thisstudy aims to compare stool sulfide concentrations incontrol and colitic subjects. Control subjects hadsignificant colorectal disease excluded by virtue of their selection. Patients with ulcerativecolitis were stratified by disease extent and activity… Expand
Decreased mucosal sulfide detoxification is related to an impaired butyrate oxidation in ulcerative colitis
TLDR
An impaired detoxification mechanism of sulfide at TST protein and RNA level in UC was found andlammation was clearly associated with the observed TST deficiency. Expand
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TLDR
The results provide a rationale for additional studies to determine whether the high sulfide production is a cause or effect of pouchitis, and suggest a fundamental difference in gut sulfide metabolism that could have implications for the etiology of ulcerative colitis as well as the pouchitis of patients with ulceratives colitis. Expand
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TLDR
Bismuth subnitrate was utilized to quantitate intracolonic sulfide release based on observations that bismuth avidly binds sulfide; quantitatively releases bound sulfide when acidified; and 3) does not influence fecal sulfide production by fecal homogenates. Expand
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TLDR
Chronic cytotoxicity of sulfide and genotoxicity using the single-cell gel electrophoresis (SCGE) in Chinese hamster ovary and HT29-Cl cells indicate that given a predisposing genetic background that compromises DNA repair, H2S may lead to genomic instability or the cumulative mutations found in adenomatous polyps leading to colorectal cancer. Expand
Hydrogen Sulfide and Colonic Epithelial Metabolism
Hydrogen sulfide (HS−) impairs the oxidation of butyrate in colonocytes and is found in excess in feces of patients with ulcerative colitis. The possible pathogenic role of HS− in ulcerative colitisExpand
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TLDR
The concept that sulfide is simply a metabolic troublemaker toward colonic epithelial cells has been challenged by the discovery that micromolar concentration of H2S is able to increase the cell respiration and to energize mitochondria allowing these cells to detoxify and to recover energy from luminal sulfide. Expand
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TLDR
Standardized breath gas measurements combined with ever-improving molecular methodologies could provide novel strategies to prevent, diagnose or manage numerous colonic disorders. Expand
Influence of Feces from Patients with Ulcerative Colitis on Butyrate Oxidation in Rat Colonocytes
TLDR
Feces from healthy subjects and patients with quiescent and active ulcerative colitis containhibitor(s) of the production of CO2 from butyrate oxidation in colonocytes, however, a specific inhibitory effect of feces from patients with ulceratives colitis on the productionof CO2 could not be identified. Expand
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TLDR
The increasing severity of inflammation along the proximal-to-distal axis in UC is due to the dilution of beneficial factors, concentration of toxic factors, and changing detoxification capacity of the host, all of which are intimately linked to the nutrient flow from the diet. Expand
Oxidation of hydrogen sulfide and methanethiol to thiosulfate by rat tissues: a specialized function of the colonic mucosa.
TLDR
It is concluded that colonic mucosa possesses a specialized detoxification system that allows this tissue to rapidly metabolize H(2)S and CH(3)SH to thiosulfate, and Presumably, this highly developed system protects the colon from what otherwise might be injurious concentrations of H( 2)S or CH( 3)SH. Expand
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