, Volume 42, Issue 8, pp 1571-1579

Colonic Sulfide in Pathogenesis and Treatment of Ulcerative Colitis

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

A role for colonic sulfide in the pathogenesisand treatment of ulcerative colitis (UC) has emergedbased on biochemical, microbiological, nutritional,toxicological, epidemiological, and therapeuticevidence. Metabolism of isolated colonic epithelial cellshas indicated that the bacterial short-chain fatty acidn-butyrate maintains the epithelial barrier and thatsulfides can inhibit oxidation of n-butyrate analogous to that observed in active UC. Sulfurfor fermentation in the colon is essential forn-butyrate formation and sulfidogenesis aids disposal ofcolonic hydrogen produced by bacteria. The numbers of sulfate-reducing bacteria and sulfidogenesisis greater in UC than control cases. Sulfide is mainlydetoxified by methylation in colonic epithelial cellsand circulating red blood cells. The enzyme activity of sulfide methylation is higher in red bloodcells of UC patients than control cases. Patients withUC ingest more protein and thereby sulfur amino acidsthan control subjects. Removing foods rich in sulfur amino acids (milk, eggs, cheese) has proventherapeutic benefits in UC. 5-Amino salicylic acidreduces fermentative production of hydrogen sulfide bycolonic bacteria, and aminoglycosides, which inhibit sulfate-reducing bacteria, are of therapeuticbenefit in active UC. Methyl-donating agents are acategory of drugs of potential therapeutic use in UC. Acorrelation between sulfide production and mucosal immune responses in UC needs to be undertaken.Control of sulfidogenesis and sulfide detoxification maybe important in the disease process of UC, althoughwhether their roles is in an initiating or promoting capacity has yet to be determined.