Hydrogen sulfide and colonic epithelial metabolism: implications for ulcerative colitis

Dig Dis Sci. 2001 Aug;46(8):1722-32. doi: 10.1023/a:1010661706385.


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 colitis was further investigated. To investigate the metabolic effect of free and bound fecal HS-, isolated rat colonocytes were incubated in the presence of butyrate without and with the addition of (1) HS- in water, (2) sterile filtrates of fecal homogenates supplemented and incubated with HS- and known sources of fecal HS- production, and (3) HS- incubated with fecal agents known to bind HS-. Oxidation rates were obtained by quantifying the production of CO2. Total and free HS-, as well as the fecal ability to bind HS-, were determined in health and ulcerative colitis. Compared to the production of CO2 by colonocytes incubated with 2 mmol/liter of butyrate, the further addition of 1.25 and 2.5 mmol/liter of HS- in water reduced the production of CO2 by 57.6+/-10.0 and 98.9+/-1.4%, respectively. However, when adding fecal filtrate of homogenate supplemented with HS- corresponding to 1.25 and 2.5 mmol/liter of HS- in water, the reduction of CO2 production was only 30.7+/-12.0 and 53.2+/-14.0%, respectively. Neither the fecal level of total or free HS- nor the remarkable fecal ability to bind HS- differed in health or quiescent and active ulcerative colitis. Bound HS- had no or little effect on CO2 production. Addition of fecal filtrate of nonsupplemented homogenate to colonocytes significantly reduced the oxidation of butyrate to CO2 about 25%, which could not be ascribed to fecal HS-. In conclusion, 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. Other fecal agents seem to be more potent metabolic inhibitors than fecal HS-. The role of colonic contents in the pathogenesis of ulcerative colitis remains circumstantial.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Butyrates / pharmacology
  • Carbon Dioxide / metabolism
  • Colitis, Ulcerative / metabolism*
  • Colon / cytology
  • Colon / metabolism*
  • Feces / chemistry
  • Female
  • Humans
  • Hydrogen Sulfide / analysis
  • Hydrogen Sulfide / metabolism*
  • Hydrogen Sulfide / pharmacology
  • In Vitro Techniques
  • Intestinal Mucosa / metabolism*
  • Ketone Bodies / metabolism
  • Male
  • Middle Aged
  • Oxidation-Reduction
  • Rats
  • Rats, Sprague-Dawley


  • Butyrates
  • Ketone Bodies
  • Carbon Dioxide
  • Hydrogen Sulfide