Colonic Luminal Hydrogen Sulfide Is Not Elevated in Ulcerative Colitis

  title={Colonic Luminal Hydrogen Sulfide Is Not Elevated in Ulcerative Colitis},
  author={J W Moore and Wendy J Babidge and Susan Millard and William E W Roediger},
  journal={Digestive Diseases and Sciences},
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… 
Decreased mucosal sulfide detoxification is related to an impaired butyrate oxidation in ulcerative colitis
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.
Association Between Fecal Hydrogen Sulfide Production and Pouchitis
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.
Physiology of sulfide in the rat colon: use of bismuth to assess colonic sulfide production.
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.
Evidence That Hydrogen Sulfide Is a Genotoxic Agent
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.
Hydrogen Sulfide and Colonic Epithelial Metabolism
Fecal HS− has little effect on butyrate oxidation in colonocytes and does not seem to play a pathogenic role for UC by impairing colonic epithelial metabolism, while other fecal agents seem to be more potent metabolic inhibitors than fecal HS −.
Luminal sulfide and large intestine mucosa: friend or foe?
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.
Contributions of the microbial hydrogen economy to colonic homeostasis
Standardized breath gas measurements combined with ever-improving molecular methodologies could provide novel strategies to prevent, diagnose or manage numerous colonic disorders.
Influence of Feces from Patients with Ulcerative Colitis on Butyrate Oxidation in Rat Colonocytes
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.
Dietary Factors in Sulfur Metabolism and Pathogenesis of Ulcerative Colitis
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.


Butyrate oxidation is impaired in the colonic mucosa of sufferers of quiescent ulcerative colitis.
Data confirm that in quiescent ulcerative colitis there is an impairment of butyrate oxidation, which is significantly impaired compared with that in normal mucosa.
Sulphide impairment of substrate oxidation in rat colonocytes: a biochemical basis for ulcerative colitis?
A hypothesis for the disease process of ulcerative colitis is that sulphides may form persulphides with butyryl-CoA, which would inhibit cellular short-chain acyl- CoA deHydrogenase and beta-oxidation to induce an energy-deficiency state in colonocytes and mucosal inflammation.
Hydrogen sulphide and total acid-volatile sulphide in faeces, determined with a direct spectrophotometric method.
  • T. Florin
  • Biology
    Clinica chimica acta; international journal of clinical chemistry
  • 1991
Therapeutic benefits from a poorly absorbed prednisolone enema in distal colitis.
There are theoretical advantages in using a poorly absorbed enema to avoid the possibility of systemic steroid effects in patients requiring long term steroid treatment.
Salicylate s inhibit bacterial sul® de production within the colonic lumen in ulcerative colitis
  • Gut 37(suppl 2) :A15, 1995 HYDROGEN SULFIDE IN ULCERATIVE COLITIS 165 Digestive Diseases and Sciences, Vol. 43, No. 1
  • 1998
Sulfur metabolism in colons of carrage enan fed rats
  • J Gastroente rol Hepatol 10:A56,
  • 1995
A role for sulphate reducing bacteria in ulcerative colitis
  • Gastroenterology 98:A170,
  • 1990
Incidence and activities of sulfate reducing bacteria in patients with ulcerative colitis
  • Gut 36(suppl 1)
  • 1995