ArticleGut2005
Diffusion of cytotoxic concentrations of nitric oxide generated luminally at the gastro-oesophageal junction of rats.
Article in Gut, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 39 citations in OpenAlex.
- Estrogen-Dependent Nrf2 Expression Protects Against Reflux-Induced Esophagitis.Digestive diseases and sciences · 2018Article
- Role of nitric oxide in the pathogenesis of Barrett's-associated carcinogenesis.World journal of gastrointestinal pathophysiology · 2016Review
- The redox interplay between nitrite and nitric oxide: From the gut to the brain.Redox biology · 2013Review
- Role of gastric acid secretion in the pathogenesis of Barrett's esophageal cancer in a Japanese population.Clinical journal of gastroenterology · 2009Article
- Enhancement of esophageal carcinogenesis in acid reflux model rats treated with ascorbic acid and sodium nitrite in combination with or without initiation.Cancer science · 2008Article
- NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS.The Journal of clinical investigation · 2007Article
- Combined treatment with green tea catechins and sodium nitrite selectively promotes rat forestomach carcinogenesis after initiation with N-methyl-N'- nitro-N-nitrosoguanidine.Cancer science · 2007Article
- Gastric carditis: Is it a histological response to high concentrations of luminal nitric oxide?World journal of gastroenterology · 2006Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn humans, high concentrations of nitric oxide are generated luminally at the gastro-oesophageal junction through enterosalivary recirculation of dietary nitrate.
aimTo investigate whether luminal nitric oxide can diffuse into the adjacent digestive tissue and alter tissue integrity.
methodsWe designed an animal model using Wistar rats in which physiological concentrations of nitrite and acidified ascorbic acid were administered separately so that the two reactants first meet to form nitric oxide at the gastro-oesophageal junction. Luminal and tissue concentrations of nitric oxide were measured with an electrode and an electron paramagnetic resonance spectrometer, respectively. Concentrations of glutathione in the tissue were measured as a marker of nitrosative stress.
resultsHigh concentrations of luminal nitric oxide were generated locally at the gastro-oesophageal junction of nitrite administered rats, reproducing a phenomenon observed in humans. High levels of nitric oxide were also detected largely in the superficial epithelium of the gastro-oesophageal junction. The concentration of tissue glutathione at the gastro-oesophageal junction was significantly lower in nitrite administered rats compared with control rats, whereas that in the distal stomach was similar in the two rat groups.
conclusionsUsing an animal model, this study demonstrated that nitric oxide generated in the lumen diffuses into the adjacent gastric tissue to a substantial degree, leading to localised consumption of glutathione in the tissue. Nitrosative stress induced by this mechanism may be involved in the high prevalence of inflammation and metaplasia, and subsequent development of neoplastic disease at this site.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.