Digestive Diseases and Sciences

, Volume 46, Issue 8, pp 1722–1732

Hydrogen Sulfide and Colonic Epithelial Metabolism

  • Jimmy Jørgensen
  • Per Brøbech Mortensen

DOI: 10.1023/A:1010661706385

Cite this article as:
Jørgensen, J. & Mortensen, P.B. Dig Dis Sci (2001) 46: 1722. 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.

hydrogen sulfideulcerative colitisbutyratefecescolonocytedetoxification

Copyright information

© Plenum Publishing Corporation 2001

Authors and Affiliations

  • Jimmy Jørgensen
    • 1
  • Per Brøbech Mortensen
    • 1
  1. 1.Department of Medicine CA 2121, Section of GastroenterologyCopenhagen University Hospital, The RigshospitalCopenhagenDenmark