Ascorbic acid in the human stomach

Sobala, G. M.; Schorah, C. J.; Sanderson, Marion; Dixon, M. F.; Tompkins, David; Godwin, P. G. R.; Axon, Anthony

doi:10.1016/0016-5085(89)90071-1

Cited by 195 publications

(97 citation statements)

References 17 publications

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“…Ascorbic acid is actively secreted in the stomach [17,30] and has the capacity to reduce HNO 2 to U NO and inhibit the local formation of N-nitrosamines [31,32]. Thus, caffeic acid and other wine phenols have to compete with ascorbic acid, an intrinsic reductant of gastric juice, for nitrite.…”

Section: Production Of Nitric Oxide From Nitrite Promoted By Red Winementioning

confidence: 99%

“…It has been reported that ascorbic acid (pK 1 = 4.1), upon interaction with nitrite, is oxidized to dehydroascorbate and intermediary radicals are expected to be formed [7,17,32,33]. Similarly to ascorbic acid, caffeic acid is known as an antioxidant which in view of its redox properties is capable to reduce several compounds, including vitamin E radical [34].…”

Section: μM (Line 4)mentioning

confidence: 99%

“…Ascorbic acid, exhibiting a low redox potential (0.28 V) and actively secreted in the gastric juice is an obvious candidate [16,17]. Yet, dietary polyphenols that, depending on its structure, have been shown to redox interact with oxidant radicals, thus preventing oxidative reactions, may be present in large amounts in the stomach in a diet-dependent way and likely promote U NO formation at high fluxes.…”

Section: Introductionmentioning

confidence: 99%

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Red wine-dependent reduction of nitrite to nitric oxide in the stomach

Gago

Lundberg

Barbosa

et al. 2007

Free Radical Biology and Medicine

159

111

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Nitrite may be a source for nitric oxide ( U NO), particularly in highly acidic environments, such as the stomach. Diet products contribute also with reductants that dramatically increase the production of U NO from nitrite. Red wine has been attributed health promoting properties largely on basis of the reductive antioxidant properties of its polyphenolic fraction. We show in vitro that wine, wine anthocyanin fraction and wine catechol (caffeic acid) dose-and pH-dependently promote the formation of U NO when mixed with nitrite, as measured electrochemically. The production of U NO promoted by wine from nitrite was substantiated in vivo in healthy volunteers by measuring U NO in the air expelled from the stomach, following consumption of wine, as measured by chemiluminescence. Mechanistically, the reaction involves the univalent reduction of nitrite, as suggested by the formation of U NO and by the appearance of EPR spectra assigned to wine phenolic radicals. Ascorbic and caffeic acids cooperate in the reduction of nitrite to U NO. Moreover, reduction of nitrite is critically dependent on the phenolic structure and nitro-derivatives of phenols are also formed, as suggested by caffeic acid UV spectral modifications. The reduction of nitrite may reveal previously unrecognized physiologic effects of red wine in connection with U NO bioactivity.

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Section: Production Of Nitric Oxide From Nitrite Promoted By Red Winementioning

confidence: 99%

Section: μM (Line 4)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Red wine-dependent reduction of nitrite to nitric oxide in the stomach

Gago

Lundberg

Barbosa

et al. 2007

Free Radical Biology and Medicine

159

111

View full text Add to dashboard Cite

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“…In vitro studies suggest that these concentrations of nitrite and acid would generate about one tenth of the NO that is actually measured (McKnight, Smith and Benjamin, unpublished data). It is likely that a reducing substance such as ascorbic acid [32][33][34], which is actively secreted into the stomach, or reduced thiols (which are in high that which we would predict would be necessary to generate the amount of nitric oxide release we observed from the skin. The source of nitrite is not clear, but is likely to be from bacterial reduction of sweat nitrate by skin commensal organisms which are known to elaborate the nitrate reductase enzyme.…”

Section: Acidification Of Nitrite -Production Of No In the Mouth And mentioning

confidence: 86%

Nitrates in the human diet - good or bad?

Benjamin

2000

Ann. Zootech.

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-Although the nitrate and nitrite have been used for centuries, it has only recently been discovered that nitrate is manufactured in mammals by the oxidation of nitric oxide and that the nitrate formed also has the potential for disinfecting the food we eat. The mechanisms by which nitric oxide and other nitrogen oxides provide selective toxicity towards pathogens is not yet completely understood, and it is likely that the mechanisms will be different with different organisms. Whereas it is clear that acidified nitrite is produced on mucosal surfaces, and that this combination is effective in killing a variety of human gut and skin pathogens, there is no definite evidence as yet that this mechanism is truly protective in humans exposed to a contaminated environment. Further understanding of the complex chemistry of nitrogen oxides may also help develop new antimicrobial therapies based on augmenting what seems to be a simple and effective host defence system. nitrates / nitrites / human diet / healthRésumé -Les nitrates dans l'alimentation humaine : une bonne ou une mauvaise chose ? Bien que les nitrates soient connus depuis des siècles, c'est seulement depuis peu qu'il a été décou-vert que les nitrates sont synthétisés chez les mammifères à partir du monoxyde d'azote, et que les nitrates formés ont la capacité de tuer les bactéries présentes dans les aliments consommés. Les mécanismes par lesquels le monoxyde d'azote et d'autres oxydes d'azote manifestent une toxicité sélec-tive vis-à-vis de bactéries pathogènes ne sont pas encore totalement élucidés. Il est probable que ces mécanismes dépendent des organismes considérés. Alors qu'il est clair que les nitrites acidifiés sont produits à la surface des muqueuses, et que cela permet de tuer de nombreux agents pathogènes de la peau et de l'intestin de l'Homme, une incertitude demeure quant aux mécanismes de protection réels de l'Homme exposé à un environnement contaminé. Une meilleure compréhension de la chimie complexe des oxydes d'azote permettra d'aider au développement de nouvelles thérapies antibacté-riennes fondées sur l'accroissement de ce qui semble être un système de défense de l'hôte simple et efficace.nitrates / nitrites / alimentation humaine / santé humaine

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“…34 Several experimental studies have demonstrated that TGF-b inhibits pentagastrin-stimulated gastric acid secretion in rats, suggesting a new mechanism of TGF-b action in gastroduodenal ulcer healing. 35 On the contrary, inhibition of gastric acid secretion results in increased gastric pH, low levels of ascorbic acid, 36 a diminished ability to block the endogenous formation of N-nitroso compounds 37 and a higher risk of GC. Based on these data, the different distribution of TGFB1 þ 869 genotypes between DU and GC patients observed in our study, besides supporting the concept of a different genetic background for both entities, might help explain, at least in part, how H. pylori can induce such divergent outcomes, in this case by regulating homeostasis of gastric acid secretion.…”

Section: Discussionmentioning

confidence: 99%

TGFB1 gene polymorphisms: their relevance in the susceptibility to Helicobacter pylori-related diseases

et al. 2006

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Recent studies have revealed elevated expression of transforming growth factor b1 (TGF-b1) in gastric mucosa of patients with gastric cancer (GC) and those undergoing ulcer repair. As production of TGF-b1 is genetically regulated, we aimed to assess whether functional polymorphisms of the TGFB1 gene are involved in susceptibility to and clinical characteristics of Helicobacter pylori-related diseases. DNA from 142 unrelated Spanish patients with GC, 200 with peptic ulcer and 342 healthy controls was typed for the MspA1I T þ 869C, and the Sau96I G þ 915C polymorphisms of the TGFB1 gene using polymerase chain reaction and RFLP analysis. H. pylori infection and CagA/VacA antibody status were determined by Western blot in patients and controls. H. pylori infection (odds ratio (OR): 11.44; 95% confidence interval (CI): 4.45-29.42; Po0.001) and nonsteroidal anti-inflammatory drugs (OR: 5.07; 95% CI: 2.53-10.16; Po0.001) were identified as independent risks factors for duodenal ulcer (DU), whereas the TGFB1 þ 869*C/C genotype was associated with reduced risk of developing the disease (OR: 0.32; 95% CI ¼ 0.15-0.68; P ¼ 0.003). Our results show that the TGFB1 T þ 869C gene polymorphism is involved in the susceptibility to DU and provide further evidence that host genetic factors play a key role in the pathogenesis of H. pylorirelated diseases.

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Ascorbic acid in the human stomach

Cited by 195 publications

References 17 publications

Red wine-dependent reduction of nitrite to nitric oxide in the stomach

Red wine-dependent reduction of nitrite to nitric oxide in the stomach

Nitrates in the human diet - good or bad?

TGFB1 gene polymorphisms: their relevance in the susceptibility to Helicobacter pylori-related diseases

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