Effect of vitamin E in gastric mucosal injury induced by ischaemia‐reperfusion in nitric oxide‐depleted rats

Naito,; Yoshikawa,; Matsuyama,; Yagi,; Kasai,; Sugimoto,; Masui,; Yoshida, Minoru; Kondo,

doi:10.1046/j.1365-2036.1999.00480.x

Cited by 10 publications

(6 citation statements)

References 15 publications

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“…More and more evidence suggests that the majority of injuries occur during reperfusion [3][4][5], and this may be attributable to reactive oxygen metabolites initially generated at the level of the vasculature [6]. Sources of reactive oxygen metabolites in reperfusing tissues include the xanthine oxidase system, which produces superoxides and hydrogen peroxides during reperfusion [7,8], and activated neutrophils, which infiltrate into the tissues and bind to the microvascular endothelium [9,10].…”

Section: Introductionmentioning

confidence: 99%

Role of Nitric Oxide and Mucus in Ischemia/Reperfusion-Induced Gastric Mucosal Injury in Rats

Kim¹,

Kim²

2001

Pharmacology

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The present study aims at investigating the role of nitric oxide (NO) on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion (I/R) and its relation to mucus. NO synthesis modulators such as L-arginine and N^G-nitro-L-arginine methyl ester (L-NAME) were injected intraperitoneally to the rats 30 min prior to I/R which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. As a result, I/R increased lipid peroxide production and decreased the contents of glutathione (GSH), cGMP and mucus as well as GSH peroxidase activities of gastric mucosa. I/R decreased the activity and protein of NO synthase (NOS) in gastric mucosa. Pretreatment of L-arginine, a substrate for NOS, prevented I/R-induced alterations of gastric mucosa. However, L-NAME, an NOS inhibitor, deteriorated oxidative damage induced by I/R. In conclusion, NO has an antioxidant defensive role on gastric mucosa by maintaining mucus, GSH and GSH peroxidase, which were related to preservation of cGMP and NOS in gastric mucosa.

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Section: Introductionmentioning

confidence: 99%

Role of Nitric Oxide and Mucus in Ischemia/Reperfusion-Induced Gastric Mucosal Injury in Rats

Kim¹,

Kim²

2001

Pharmacology

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“…[16][17][18][19][20] Naito et al 22) have shown that vitamin E protects against ischemia-reperfusioninduced gastric mucosal injury under nitric oxide depletion in rats by inhibiting not only lipid peroxidation but also neutrophil infiltration in the gastric mucosal tissue. We have reported that neutrophil infiltration into gastric mucosal tissues contributes to not only the formation but also the progression of C48/80-induced acute gastric mucosal lesions in rats.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18][19][20] Yoshikawa et al 21) reported that both a decrease in gastric mucosal vitamin E level and an increase in gastric mucosal lipid peroxidation occurred during the development of ischemia-reperfusion-induced gastric mucosal injury in rats and that the severity of ischemia-reperfusion-induced gastric mucosal injury was enhanced in vitamin E-deficient rats. Naito et al 22) have shown in nitric oxide-depleted rats that vitamin E plays an important role in protecting against ischemia-reperfusion-induced gastric mucosal injury, and have suggested that this gastroprotective effect of vitamin E is due to not only its antioxidant action but also its inhibitory action on neutrophil infiltration into the gastric mucosa. Al-Dhohyan and Al-Tuwaijri 23) reported that a single oral pre-admin- The effect of oral vitamin E administration on acute gastric mucosal lesion progression was examined in rats treated once with compound 48/80 (C48/80) (0.75 mg/kg, i.p.)…”

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confidence: 99%

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

Ohta

Kobayashi

Imai

et al. 2006

Biological & Pharmaceutical Bulletin

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Compound 48/80 (C48/80) is known to cause degranulation of connective tissue mast cells, but not mucosal mast cells, with release of serotonin and histamine from the cells. 1,2) We have shown in rats with a single C48/80 treatment that the development of gastric mucosal lesions occurs with decreases in Se-glutathione peroxidase (Se-GSHpx) activity and vitamin E and hexosamine levels and increases in neutrophil infiltration, xanthine oxidase (XO) activity, and lipid peroxide level in the gastric mucosal tissue and that gastric mucosal blood flow changes like ischemia-reperfusion during gastric mucosal lesion development.3) We have also shown in rats treated once with C48/80 that neutrophils infiltrating into the gastric mucosal tissue participate in gastric mucosal lesion formation and progression, while the xanthine-XO system in the gastric mucosal tissue takes part mainly in the lesion progression. 4) Furthermore, it has been shown in rats treated once with C48/80 that acutely released endogenous serotonin contributes to gastric mucosal lesion formation, while released endogenous histamine mainly contributes to the lesion progression, although gastric acid plays no important role in the pathogenesis of the C48/80-induced gastric mucosal lesion.3,5) Ascorbic acid (vitamin C) is a water-soluble antioxidant and it scavenges reactive oxygen species (ROS), such as superoxide radical (O 2 Ϫ ), hydroxyl radical (OH . ), hydrogen peroxide (H 2 O 2 ), singlet oxygen, and hypochlorus acid, by itself and also supports the chainbreaking antioxidant action of vitamin E by reducing vitamin E radical to vitamin E at the liquid/aqueous interface. [6][7][8][9][10][11] In addition, ascorbic acid prevents neutrophil adherence to endothelium by scavenging ROS derived from activated neutrophils.12) Our recent reports have shown that ascorbic acid content decreases with a concomitant decrease in vitamin E content during lesion progression in the gastric mucosa of rats treated once with C48/80 and that gastric mucosal ascorbic acid plays a critical role in the progression of C48/80-induced gastric mucosal lesions, which is closely associated with its antioxidant and anti-inflammatory actions in the gastric mucosa. 13,14) Vitamin E is a lipid-soluble antioxidant and it functions as a chain-breaking antioxidant for lipid peroxidation in cell membranes and also as a scavenger of ROS such O 2 Ϫ , OH . , and singlet oxygen. 15) Vitamin E exerts an anti-inflammatory action by inhibiting the production O 2 Ϫ in activated neutrophils, adhesion of neutrophils to endothelial cells, and transendothelial migration of neutrophils. [16][17][18][19][20] Yoshikawa et al. 21) reported that both a decrease in gastric mucosal vitamin E level and an increase in gastric mucosal lipid peroxidation occurred during the development of ischemia-reperfusion-induced gastric mucosal injury in rats and that the severity of ischemia-reperfusion-induced gastric mucosal injury was enhanced in vitamin E-deficient rats. Naito et al. 22) have shown in nitric oxide-depl...

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“…Hypovolemia-related injury has not been studied adequately in animals. Currently, there are also no related human data available on this phase of tissue damage (9)(10)(11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 99%

“…Regardless of the type of irritant that damages the gastric mucosa, production of these oxygen radicals plays a role in the tissue damage. It is well established that damaged tissue contains decreased levels of antioxidant enzymes and increased levels of lipid peroxidation products (1,(9)(10)(11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 99%

Hypovolemia-related gastric tissue damage in the setting of upper gastrointestinal bleeding

Karıncaoğlu

Seçkin

Ateş³

et al. 2010

Turk J Gastroenterol

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Effect of vitamin E in gastric mucosal injury induced by ischaemia‐reperfusion in nitric oxide‐depleted rats

Abstract: These results indicate that the inhibition of lipid peroxidation and interference with neutrophil infiltration by vitamin E may be responsible for its cytoprotective effect in ischaemia-reperfusion.

Cited by 10 publications

References 15 publications

Role of Nitric Oxide and Mucus in Ischemia/Reperfusion-Induced Gastric Mucosal Injury in Rats

Role of Nitric Oxide and Mucus in Ischemia/Reperfusion-Induced Gastric Mucosal Injury in Rats

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

Hypovolemia-related gastric tissue damage in the setting of upper gastrointestinal bleeding

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