Eukaryotic and Prokaryotic Sources of Colonic Hydrogen Sulfide Synthesis
Bibliographic record
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 contributes to resolution. Some of the bacteria residing in the colon also produce H2S. The extent to which bacterial H2S synthesis contributes to what is measured as colonic H2S synthesis is not clear. When comparing conventional and germ-free mice we found no differences in colonic H2S synthesis. Furthermore, we found that colonic H2S synthesis is markedly increased when colonic tissue is inflamed, and, in proportion to the extent of inflammation, however fecal H2S synthesis does not change. Finally, rats fed a B vitamin-deficient diet for 6 weeks 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 we measure as colonic tissue H2S production. In another study, the contributions of three enzymatic pathways to colonic H2S synthesis were determined in tissues taken from healthy rats and rats with colitis. The ability of colonic tissue to inactivate H2S was also determined. The majority of increased H2S synthesis, in both healthy and inflamed tissue, was derived via a pyroxidal-5’-phosphate-independent pathway. Ulcerated mucosal tissue accounted for the greatest levels of H2S synthesis, and the extent of granulocyte infiltration into the tissue did not appear to be a significant determinant of the levels of H2S production. Inactivation of H2S by colonic tissue occurred rapidly, but was significantly reduced in ulcerated colonic tissue from rats with colitis. Damage to colonic tissue appears to be the major stimulus for enhanced H2S synthesis. Together, the increased production and decreased inactivation of H2S may contribute to promoting resolution of inflammation and repair of damaged colonic tissue.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".