Role of oxygen radicals in ischemia-induced lesions in the cat stomach

Perry, Michael A.; Wadhwa, Surjit S.; Parks, Dale A.; Pickard, William F.; Granger, D. Neil

doi:10.1016/0016-5085(86)90933-9

Cited by 260 publications

(91 citation statements)

References 14 publications

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“…Oxygen-free radicals and lipid peroxidation have been reported to participate in the formation of gastric mucosal lesions caused by a variety of ulcerogenic stimuli, such as ischemia-reperfusion (Perry et al, 1986) and several kinds of stress (Ito and Guth, 1985;Yoshikawa et al, 1986;. They have been implicated in the pathogenesis of ethanol-induced gastric mucosal injury as well (Pihan et al, 1987), because two enzymatic antioxidants, superoxide dismutase, and catalase reduced the gastric mucosal injury.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, oxygen-free radicals are involved in the process of formation of gastric mucosal lesions that are induced by a variety of ulcerogenic stimuli such as ischemia-reperfusion (Perry et al, 1986), several kinds of stress (Ito and Guth, 1985;Yoshikawa et al, 1986;, and ethanol (Pihan et al, 1987), and antioxidants can afford gastric cytoprotection. In ad-dition, it has been reported that intravenous administration of MT-II (2.5 mg/kg, 1.0 mg/kg, iv) suppresses the formation of water-immersion stress-induced and HCl-ethanol-induced gastric mucosal lesions in rats (Mimura et al, 1988).…”

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confidence: 99%

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Cytoprotection by Metallothionein Against Gastroduodenal Mucosal Injury Caused by Ethanol in Mice

Takano

Satoh

Shimada

et al. 2000

Laboratory Investigation

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SUMMARY:Metallothionein (MT) is a small, cysteine-rich protein that can act as a free radical scavenger at least in vitro. To test the hypothesis that MT participates in gastroduodenal cytoprotection, we studied sensitivity to gastroduodenal mucosal injury caused by ethanol in MT-null mice that have null mutations in MT-I and MT-II genes. MT-null mice and wild-type mice were orally treated with ethanol (60% or 99.5%, 0.2 ml/mouse). The macroscopic gastric lesion indices were significantly higher in MT-null mice than in wild-type mice 90 minutes after ethanol treatment. Histopathological examination in ethanol-treated MT-null mice showed vacuolar degeneration, necrosis of the epithelial cells, and hemorrhage throughout the tunica mucosa. Moreover, the duodenum also showed morphologic changes, including marked degeneration and coagulative necrosis of the entire villi, desquamation of the degenerated epithelial cells, and hemorrhage. In contrast, histopathologic changes were less prominent in the wild-type mice treated with ethanol. MT was not detected either in the stomach or duodenum of MT-null mice, whereas gastric and duodenal zinc contents were not significantly different between MT-null mice and wild-type mice. These results provide direct evidence that intrinsic MT plays a cytoprotective role in gastroduodenal mucosal injury caused by ethanol. (Lab Invest 2000, 80:371-377).

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cytoprotection by Metallothionein Against Gastroduodenal Mucosal Injury Caused by Ethanol in Mice

Takano

Satoh

Shimada

et al. 2000

Laboratory Investigation

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“…The anti-oxidant capacity of plasma was found to be doubled by the administration of NO donors. Moreover, these concentrations of the NO donors prevented reperfusion-induced mucosal injury, which has been shown to be mediated in large part by reactive oxygen metabolites (Perry et al 1986, Zimmerman et al 1990. A mechanism for superoxide anion scavenging by NO has not been clearly delineated.…”

Section: Anti-oxidant Activitymentioning

confidence: 96%

Nitric oxide as a regulator of inflammatory processes

Wallace

2005

Mem. Inst. Oswaldo Cruz

117

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“…Due to their high reactivity and short life, it has still not been elucidated which free radicals, i.e., the superoxide or hydroxyl radical, play an important role in these mucosal lesions (1)(2)(3)(4)(5). Several investigations (6, 7) have been performed using H2O2 as the necrotizing agent.…”

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confidence: 99%

Protective Effect of Rebamipide against Hydrogen Peroxide-Induced Hemorrhagic Mucosal Lesions in Rat Stomach

Sakurai

Yamasaki

1994

Japanese Journal of Pharmacology

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ABSTRACT-Intragastric administration of 6°1o H202 induces gastric mucosal hemorrhagic lesions in rats. Intraperitoneal administration of rebamipide at 10 to 100 mg/kg dose-dependently prevented the H202 induced mucosal lesions. The fact that cimetidine, ranitidine and omeprazole could not prevent the gastric mucosa from developing H202-induced lesions indicates that acid secretion might not be the main cause of these lesions. The protective effect of rebamipide was partially reduced by indomethacin and completely blocked by diethyl maleate, a glutathione depressor. Gastric mucosal glutathione level and glutathione peroxidase and superoxide dismutase (SOD) activities were significantly decreased by 6% H202 instillation. Rebamipide at 100 mg/kg significantly inhibited the decreases in gastric mucosal glutathione level and SOD activity. These results suggest that H202-induced gastric mucosal lesions might partially involve a decrease in defense activities against reactive oxygen species and that the protective effect of rebamipide might be related to its ability to improve oxidative stress in gastric mucosa.

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Role of oxygen radicals in ischemia-induced lesions in the cat stomach

Cited by 260 publications

References 14 publications

Cytoprotection by Metallothionein Against Gastroduodenal Mucosal Injury Caused by Ethanol in Mice

Cytoprotection by Metallothionein Against Gastroduodenal Mucosal Injury Caused by Ethanol in Mice

Nitric oxide as a regulator of inflammatory processes

Protective Effect of Rebamipide against Hydrogen Peroxide-Induced Hemorrhagic Mucosal Lesions in Rat Stomach

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