Eukaryotic and prokaryotic contributions to colonic hydrogen sulfide synthesis

Abstract

Hydrogen sulfide (H2S) is an important modulator of many aspects of digestive function, both in health and disease. Colonic tissue H2S synthesis increases markedly during injury and inflammation and appears to contribute to resolution. Some of the bacteria residing in the colon can also produce H2S. The extent to which bacterial H2S synthesis contributes to what is measured as colonic H2S synthesis is not clear. Using conventional and germ-free mice, we have delineated the eukaryotic vs. prokaryotic contributions to colonic H2S synthesis, both in healthy and colitic mice. Colonic tissue H2S production is entirely dependent on the presence of the cofactor pyridoxal 5′-phosphate (vitamin B6), while bacterial H2S synthesis appears to occur independent of this cofactor. As expected, approximately one-half of the H2S produced by feces is derived from eukaryotic cells. While colonic H2S synthesis is markedly increased when the tissue is inflamed, and, in proportion to the extent of inflammation, fecal H2S synthesis does not change and tissue granulocytes do not appear to be the source of the elevated H2S production. Rats fed a B vitamin-deficient diet for 6 wk exhibited significantly diminished colonic H2S synthesis, but fecal H2S synthesis was not different from that of rats on the control diet. Our results demonstrate that H2S production by colonic bacteria does not contribute significantly to what is measured as colonic tissue H2S production, using the acetate trapping assay system employed in this study.