ArticleDigestive diseases and sciences1994
Studies on peroxisomes of colonic mucosa in Crohn's disease.
Article in Digestive diseases and sciences, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Catalase inhibition can modulate the ability of peripheral blood T cells to undergo apoptosis in Crohn's disease.Clinical and experimental immunology · 2024Article
- The Genetic Diversity and Dysfunctionality of Catalase Associated with a Worse Outcome in Crohn's Disease.International journal of molecular sciences · 2022Article
- Functional Analyses of the Crohn's Disease Risk Gene LACC1.PloS one · 2016Article
- Crohn's disease: evidence for involvement of unregulated transcytosis in disease etio-pathogenesis.World journal of gastroenterology · 2011Review
- Altered gut transcriptome in spondyloarthropathy.Annals of the rheumatic diseases · 2006Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology and pathogenesis of Crohn's disease, a chronic inflammatory bowel pathology, have not been elucidated yet. In particular, the behavior of peroxisomes in inflamed colonic mucosa has not been investigated despite their important role in cellular oxidative metabolism. Using cytochemistry at the ultrastructural level, we have observed these catalase-positive organelles. In addition, biochemical analyses have revealed the specific activities of catalase and cyanide-insensitive acyl-CoA oxidase. Mucosal biopsy specimens from inflamed and noninflamed areas of Crohn's patients were compared to control biopsies. We found that Crohn's disease was marked by an important diminution in the peroxisomal frequency per cell unit area. If catalase activity was not affected by this pathology, cyanide-insensitive acyl-CoA oxidase, an enzyme of the peroxisomal beta-oxidation system, was found diminished in inflamed and in noninflamed areas. In conclusion, our results showed that Crohn's disease is accompanied by peroxisomal modifications but the number and the enzyme activities of colonic peroxisomes are less deeply altered in Crohn's disease than during neoplasia. This fact suggests that a relation may exist between the degree of peroxisomal deficiency and the clinical severity of colonic disease.
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