4.7 Article

Hydrogen Sulfide Metabolizing Enzymes in the Intestinal Mucosa in Pediatric and Adult Inflammatory Bowel Disease

Journal

ANTIOXIDANTS
Volume 11, Issue 11, Pages -

Publisher

MDPI
DOI: 10.3390/antiox11112235

Keywords

hydrogen sulfide; H2S metabolism; inflammatory bowel disease; IBD pathogenesis; enzymatic expression

Funding

  1. Paracelsus Medical University, Salzburg, Austria
  2. [E-17/25/134-WES]

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This study found differences in the expression of H2S-metabolizing enzymes between normal aging and inflammatory bowel disease (IBD). Healthy adults and children exhibited lower expression levels of these enzymes, while adults and children with IBD tended to have even lower expression levels.
Hydrogen sulfide (H2S) is a toxic gas that has important regulatory functions. In the colon, H2S can be produced and detoxified endogenously. Both too little and too much H2S exposure are associated with inflammatory bowel disease (IBD), a chronic intestinal disease mainly classified as Crohn's disease (CD) and ulcerative colitis (UC). As the pathogenesis of IBD remains elusive, this study's aim was to investigate potential differences in the expression of H2S-metabolizing enzymes in normal aging and IBD. Intestinal mucosal biopsies of 25 adults and 22 children with IBD along with those of 26 healthy controls were stained immunohistochemically for cystathionine-gamma-lyase (CSE), 3-mercapto-sulfurtransferase (3-MST), ethylmalonic encephalopathy 1 protein (ETHE1), sulfide:quinone oxidoreductase (SQOR) and thiosulfate sulfurtransferase (TST). Expression levels were calculated by multiplication of the staining intensity and percentage of positively stained cells. Healthy adults showed an overall trend towards lower expression of H2S-metabolizing enzymes than healthy children. Adults with IBD also tended to have lower expression compared to controls. A similar trend was seen in the enzyme expression of children with IBD compared to controls. These results indicate an age-related decrease in the expression of H2S-metabolizing enzymes and a dysfunctional H2S metabolism in IBD, which was less pronounced in children.

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