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Articles in PresS, published online ahead of print December 14, 2001
J Appl Physiol, 10.1152/jap.00907.2001
Submitted on September 4, 2001
Accepted on December 5, 2001
1 Research, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN, USA
* To whom correspondence should be addressed. E-mail: levit015{at}umn.edu.
Colonic bacteria produce hydrogen sulfide, a toxic compound postulated to play a pathogenetic role in ulcerative colitis. Colonic sulfide exposure previously has been assessed via measurements of fecal sulfide concentration. However, we found that <1% of fecal sulfide of rats was free, the remainder being bound in soluble and insoluble complexes. Thus, fecal sulfide concentrations may reflect sulfide binding capacity rather than the toxic potential of feces. We utilized bismuth subnitrate to quantitate intra-colonic sulfide release based on observations that bismuth: 1) avidly binds sulfide; 2) quantitatively releases bound sulfide when acidified; and 3) does not influence fecal sulfide production by fecal homogenates. Rats ingesting bismuth subnitrate excreted 350 ± 18 µmol/day of fecal sulfide compared to 9 ± 1 µmol/day in control rats. Thus, the colon normally absorbs about 340 µmol of sulfide daily, a quantity that would produce local and systemic injury if not efficiently detoxified by the colonic mucosa. Studies utilizing bismuth should help to clarify the factors influencing sulfide production in the human colon.
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