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François Blachier Anne-Marie Davila Sabria Mimoun Pierre-Henri Benetti Calina Atanasiu Mireille Andriamihaja Robert Benamouzig Frédéric Bouillaud Daniel Tomé 《Amino acids》2010,39(2):335-347
Hydrogen sulfide (H2S) is present in the lumen of the human large intestine at millimolar concentrations. However, the concentration of free (unbound)
sulfide is in the micromolar range due to a large capacity of fecal components to bind the sulfide. H2S can be produced by the intestinal microbiota from alimentary and endogenous sulfur-containing compounds including amino
acids. At excessive concentration, H2S is known to severely inhibit cytochrome c oxidase, the terminal oxidase of the mitochondrial electron transport chain, and thus mitochondrial oxygen (O2) consumption. However, the concept that sulfide is simply a metabolic troublemaker toward colonic epithelial cells has been
challenged by the discovery that micromolar concentration of H2S is able to increase the cell respiration and to energize mitochondria allowing these cells to detoxify and to recover energy
from luminal sulfide. The main product of H2S metabolism by the colonic mucosa is thiosulfate. The enzymatic activities involved in sulfide oxidation by the colonic epithelial
cells appear to be sulfide quinone oxidoreductase considered as the first and rate-limiting step followed presumably by the
action of sulfur dioxygenase and rhodanese. From clinical studies with human volunteers and experimental works with rodents,
it appears that H2S can exert mostly pro- but also anti-inflammatory effects on the colonic mucosa. From the available data, it is tempting
to propose that imbalance between the luminal concentration of free sulfide and the capacity of colonic epithelial cells to
metabolize this compound will result in an impairment of the colonic epithelial cell O2 consumption with consequences on the process of mucosal inflammation. In addition, endogenously produced sulfide is emerging
as a prosecretory neuromodulator and as a relaxant agent toward the intestinal contractibility. Lastly, sulfide has been recently
described as an agent involved in nociception in the large intestine although, depending on the experimental design, both
pro- and anti-nociceptive effects have been reported. 相似文献
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Claire Cherbuy Claude Andrieux Edith Honvo-Houeto Muriel Thomas Catherine Ide Nathalie Druesne Catherine Chaumontet Béatrice Darcy-Vrillon Pierre-Henri Duée 《European journal of biochemistry》2004,271(1):87-95
The expression of the colonic mitochondrial 3-hydroxy 3-methyl glutaryl CoA (mHMGCoA) synthase, a key control site of ketogenesis from butyrate, is lower in germ-free (GF) than in conventional (CV) rats. In contrast, the activity of glutaminase is higher. The objective of this study was to investigate whether the intestinal flora can affect gene expression through short chain fatty acid (SCFA) and butyrate production. GF rats were inoculated with a conventional flora (Ino-CV) or with a bacterial strain producing butyrate (Clostridium paraputrificum, Ino-Cp) or not (Bifidobacterium breve, Ino-Bb). In the Ino-CV rats, mHMGCoA synthase expression was restored to the CV values 2 days after the inoculation, i.e. concomitantly with SCFA production. In the Ino-Cp group, but not in the Ino-Bb group, mHMGCoA synthase and glutaminase were expressed at the level observed in the CV rats. These data suggest that the intestinal flora, through butyrate production, could control the expression of colonic mHMGCoA synthase and glutaminase. These modifications in gene expression by butyrate in vivo seem unrelated to a modification of histone acetylation. 相似文献
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