2004
DOI: 10.3748/wjg.v10.i17.2503
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Adaptive cytoprotection through modulation of nitric oxide in ethanol-evoked gastritis

Abstract: These findings suggest that the aggravated 500 mL/L ethanol-evoked mucosal damages under gastritis condition could be due to increased inducible NO and LTC4 production in the gastric mucosa. Only 200 mL/L ethanol is truly "cytoprotective" at the surface glandular level of non-gastritis mucosa. Furthermore, the macroscopic protection of the three mild irritants involves reduction of LTC4 level in both normal and gastritis mucosa, implicating preservation of the vasculature.

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Cited by 28 publications
(20 citation statements)
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“…This protective mechanism, evoked by mild irritants, such as low doses of ethanol, seems to involve increased production of nitric oxide primarily from the constitutive isoforms of NOS and a resultant increase in blood flow [32,33]. Therefore, we may conclude that the ulcerogenic activity of NSAIDs could be attenuated in stomach, despite an inhibition of PGE 2 , by the development of cytoprotective events.…”
Section: Controlmentioning
confidence: 95%
“…This protective mechanism, evoked by mild irritants, such as low doses of ethanol, seems to involve increased production of nitric oxide primarily from the constitutive isoforms of NOS and a resultant increase in blood flow [32,33]. Therefore, we may conclude that the ulcerogenic activity of NSAIDs could be attenuated in stomach, despite an inhibition of PGE 2 , by the development of cytoprotective events.…”
Section: Controlmentioning
confidence: 95%
“…This phenomenon has been termed "adaptive cytoprotection," and it is thought to be mediated by increased production of endogenous gastric PGs by a mild irritant [5,28]. In order to study the protective mechanism of rice extract, we evaluated the effect of rice extract on gastroprotective factors including PGE 2 .…”
Section: Discussionmentioning
confidence: 99%
“…These factors include systemic stresses and the application of local irritants [1][2][3]. Alcohol consumption, for example, can produce acute hemorrhagic gastric erosions, and excessive ingestion can result in gastritis characterized by mucosal edema, subepitherial hemorrhages, cellular exfoliation, and inflammatory cell infiltration [4,5]. Ethanol reduces levels of nonprotein sulfhydryl groups, such as glutathione, thereby increasing reactive oxygen species (ROS) that have ulcerogenic activity.…”
Section: Introductionmentioning
confidence: 99%
“…12,13 Absolute ethanol is highly corrosive to the gastric mucosa and its mechanism of action on rat gastric mucosa involves superficial necrosis of gastric mucosa and release of histamine and leukotriene C4 as tissuederived mediators. Ethanol-induced gastric ulcers have been widely used for the experimental evaluation of antiulcer activities; this method of inducing gastric lesions is a rapid and convenient way of screening cytoprotective drug as anti-ulcer potency.…”
Section: Discussionmentioning
confidence: 99%