Elsevier

The Lancet

Volume 341, Issue 8843, 20 February 1993, Pages 465-466
The Lancet

SHORT REPORTS
Increased nitric oxide synthesis in ulcerative colitis

https://doi.org/10.1016/0140-6736(93)90211-XGet rights and content

Abstract

Nitric oxide (NO) is produced in tissues by NO synthase with the liberation of equimolar amounts of citrulline. Citrulline concentrations were significantly higher in rectal biopsy specimens from patients with active ulcerative colitis than in those from patients with quiescent disease or with normal histology. Incubation of biopsy samples from patients with ulcerative colitis with NG-monomethyl-L-arginine (L-NMMA) inhibited citrulline production. These findings suggest that mucosal NO biosynthesis is increased in active colitis and that NO may have a pathogenic role in ulcerative colitis.

References (11)

There are more references available in the full text version of this article.

Cited by (343)

  • Induction of Nitric-Oxide Metabolism in Enterocytes Alleviates Colitis and Inflammation-Associated Colon Cancer

    2018, Cell Reports
    Citation Excerpt :

    In addition, NO signaling is important for the host immune response and tissue repair (Brown et al., 1993; Witthöft et al., 1998). Although a substantial increase in NO signaling has been implicated in the pathogenesis of human IBD, the specific cellular origin of NO and the exact roles of epithelial and immune cell-derived NO in intestinal inflammation remain unclear (Boughton-Smith et al., 1993; Kolios et al., 2004; Middleton et al., 1993; Suschek et al., 2004). A primary reason for the limited understanding of the role of cell- and context-dependent NO signaling in IBD is the redundancy of the three isoforms of nitric oxide synthase (NOS): endothelial (eNOS), neuronal (nNOS), and inducible (iNOS).

  • Outlier based literature exploration for cross-domain linking of Alzheimer's disease and gut microbiota

    2017, Expert Systems with Applications
    Citation Excerpt :

    This finding is coherent with the knowledge that iNOS is an important well-known mediator of brain and gut inflammation pathologies. In particular, microscopy analysis gut biopsies from human patients affected by acute gut inflammation, identified higher iNOS expression respect to healthy control subjects (Kolios, Rooney, Murphy, Robertson, & Westwick, 1998; Middleton, Shorthouse, & Hunter, 1993). iNOS was not found in gut non-inflamed samples.

View all citing articles on Scopus
View full text