Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of tissue-type plasminogen activator (t-PA) was investigated in the gastric ulcer formation induced by microvascular derangement. The rat stomach was exposed and repeated electrical stimuli (irritation) were applied on the small arterial wall close to the lesser curvature to induce mucosal ischemia followed by hyperemia. The t-PA activity in the regional blood of the stomach was significantly elevated as early as 5 min after the irritation. Immunohistochemical study using anti-t-PA monoclonal antibody revealed that t-PA was detectable in the endothelial cells of capillaries and collecting venules, suggesting the involvement of endothelium-mediated fibrinolytic activity in the irritation-induced ulcer formation. Pretreatment of SOD or allopurinol significantly attenuated the irritation-induced t-PA activation, suggesting that the t-PA activity was modulated by xanthine oxidase-associated superoxide anions. CV-6209, a selective antagonist of platelet-activating factor (PAF), also prevented the activation of t-PA as well as ulcer formation, providing a concept that PAF may be associated with the local fibrinolytic activation which may cause hemorrhagic changes in the gastric mucosal microvasculature. The present study supports the hypothesis that increased t-PA activity may reflect the microvascular endothelial damages caused by vasomotor derangement and suggests that oxygen-derived free radicals may participate in the regulation of endothelium-derived fibrinolytic activities in the mucosal microvasculature.
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PMID:Involvement of superoxide anion and platelet-activating factor in increased tissue-type plasminogen activator during rat gastric microvascular damages. 165 Sep 66

Diethyldithiocarbamate (DDC) was injected subcutaneously in the rat and the mechanism of gastric ulcer formation was investigated. DDC induced gastric ulcers in a dose-dependent manner. DDC significantly suppressed gastric mucosal copper-zinc superoxide dismutase (Cu, Zn-SOD) activity at 2 hr. However, manganese-superoxide dismutase (Mn-SOD) activity was not changed. Gastric mucosal blood flow (GMBF) decreased to 52% of the control level at 2 hr after administration of DDC and gradually increased to reach the control level by 7 hr. A Shay rat preparation (4 hr) was used to study gastric secretion. DDC (200, 400 and 800 mg/kg) inhibited acid secretion to about 80% of the control level. Histopathological examination of the gastric mucosa after administration of DDC revealed mucosal congestive findings from 1 hr to 3 hr. These data suggested that the mechanism of DDC-induced gastric ulcer formation may be attributable to a decreased level of GMBF and O2- production owing to decreased SOD activity.
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PMID:Mechanism of diethyldithiocarbamate-induced gastric ulcer formation in the rat. 215 49

The activity of enzymes of the antioxidant system and pO2 in the gastric mucosa (GM) was studied in patients with gastric ulcer. The various enzymes differed in activity. Along with low activity of superoxide dismutase (SOD), glutathione peroxidase (GP), and glutathione reductase (GR), both normal and increased values were encountered. In GM hypoxia the GP activity increased in the peri-ulcerous zone. There was no statistically significant increase of SOD activity and reduction of GR activity.
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PMID:[Enzyme activity of the gastric mucosal antioxidant system during hypoxia]. 229 63

The aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.
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PMID:The free radical mechanisms in beta-carotene induced gastric cytoprotection in HCl model. 259 22

The mucosal superoxide dismutase (SOD) activities were serially examined on the acute gastric mucosal lesion (AGML) induced by water-immersion restraint stress to rats for six hours. The mucosal SOD activities gradually increased in proportion to the time up to 3 hours after the restraint stress. But it decreased 6 hours after when severe damage had been established in the mucosa. On the other hand, the mucosal SOD activities of the margins of human gastric ulcer showed to be higher on the healing stage than on the active stage. And the SOD activities of the intractable ulcer were lower than those of the curable ulcer. These results indicate that the mucosal SOD may play some important roles both on the protecting process information of AGML and on the healing process in gastric ulcer.
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PMID:[Changes in mucosal superoxide dismutase activities of gastric lesions]. 260 64

Diethyldithiocarbamate (DDC), an inhibitor of Cu,Zn-superoxide dismutase (SOD), at a dose of 500 mg/kg or aminotriazole (AT), an inhibitor of catalase, at a dose of 2,000 mg/kg reduced slightly gastric mucosal SOD activity, did not change gastric mucosal blood flow (GMBF), and did not cause gastric ulcers. However, when both DDC and AT were administered together, gastric mucosal SOD activity and GMBF remarkably decreased, and gastric ulcers appeared. Moreover, the administration of SOD attenuated gastric ulcer induced by DDC plus AT. These results suggested that SOD may play an important role in the gastric mucosal defense mechanisms against active oxygen species.
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PMID:Gastric mucosal protection and superoxide dismutase. 284 84

Effects of treatment with free radical scavengers in the healing process of acetic acid-induced gastric ulcer on the ulcer aggravation induced by indomethacin were investigated. Gastric ulcers were produced on the anterior wall of the stomach of male Sprague-Dawley rats by submucosal injection of 20% acetic acid. To investigate the role of oxygen radicals, rats with gastric ulcer were treated with scavengers for six weeks and then treated with indomethacin (1 mg/kg/day). While superoxide dismutase (10,000 units/kg/day) did not affect the ulcer area after indomethacin treatment, allopurinol (50 mg/kg/day) slightly inhibited the increase in ulcer area. Dimethyl sulfoxide (1% solution, ad libitum) produced a significant decrease in size of the ulcer after indomethacin treatment. Increased lipid peroxides in the gastric mucosa after indomethacin treatment decreased significantly in the rats of the dimethyl sulfoxide and allopurinol groups. These results indicate that lipid peroxidation mediated by oxygen radicals plays an important role in the mechanism of ulcer aggravation induced by indomethacin.
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PMID:Effects of free radical scavengers on indomethacin-induced aggravation of gastric ulcer in rats. 755 59

Peroxidative tissue damage has been reported to contribute to several pathological disorders. Despite high exposure to both exogenous and endogenous oxidant stress, the strong cell defence mechanism of the gastric mucosa protects mucosal epithelial cells against these noxious stimuli. However, some environmental factors involved in lipid peroxidation (such as cadmium), which disrupt gastric mucosal protection, may impair the mucosal barrier and facilitate the occurrence of gastric ulcers. In an experimental study to investigate this hypothesis, the level of cadmium-induced lipid peroxidation products (TBARS) and an antioxidant enzyme (SOD) were investigated. The mucin content (P < 0.01) and prostaglandin levels (P < 0.05) of mucosa as components of the gastric mucosal barrier were found to be significantly reduced in rats exposed to 15 ppm of cadmium in water for 30 days when compared with those of unexposed controls. TBARS levels in blood (P < 0.05) and mucosa (P < 0.001) increased markedly in cadmium-exposed animals whereas blood SOD levels remained unchanged. The significant correlation between TBARS and mucosal cadmium (r = 0.664, P < 0.01), as well as between cadmium and PGE2 (r = -0.719, P < 0.01), led to the conclusion that cadmium-induced lipid peroxidation is involved in the increased vulnerability of gastric mucosa to injurious stimuli in rats. This susceptibility may be responsible for the high incidence of stress-induced gastric ulcer in the population.
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PMID:Role of lipid peroxidation in cadmium-induced impairment of the gastric mucosal barrier. 792 76

The pathogenesis of gastric mucosal injury is still poorly understood. Recent reports implicate redox active metals and reactive oxygen species as mediators of gastric damage induced by ethanol or non-steroidal anti-inflammatory drugs. Attempts were made therefore to prevent gastric injury using chelators and the antioxidant enzymes catalase and superoxide dismutase. These attempts, at best, would only detoxify extracellular reactive species, such as those produced by activated circulating granulocytes and macrophages. This study utilises another strategy by pre-emption of both intra and extracellular reactive species using radical-radical annihilation reactions and by detoxifying redox active transition metals. Nitroxide, stable free radicals were shown to enter mucous cells, protect against the ethanol induced damage, and prevent gastric lesions induced by aspirin, indomethacin, 25% NaCl, or 0.6 N HCl. These findings confirm that gastric mucosal damage from the above agents is mediated by free radicals and, moreover, introduce a prototypical agent within a potential new class of gastric ulcer preventing drugs.
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PMID:A novel antiulcerogenic stable radical prevents gastric mucosal lesions in rats. 795 22

We developed a new gastric ulcer model in which the ulcers are induced by the local injection of a ferrous iron and ascorbic acid (Fe/ASA) solution into the gastric wall. These ulcers resemble human gastric ulcers that penetrate the muscularis mucosa. The involvement of oxygen radical-mediated lipid peroxidation as the cause of these ulcers was investigated. With ferrous iron or ascorbic acid alone, gastric ulcers did not form, whereas penetrating ulcers were produced by the simultaneous injection of the Fe/ASA solution in a dose-dependent manner. Lipid peroxides significantly accumulated in the gastric mucosa from 1 to 24 h after the injection of the Fe/ASA solution. This increase in lipid peroxides preceded grossly evident gastric ulcer. Treatment with superoxide dismutase (SOD, recombinant human CuZnSOD) significantly reduced the size of the ulcers and inhibited the accumulation in lipid peroxides in the gastric mucosa, while treatment with apo-SOD or heat-inactivated SOD did not. These results suggest that lipid peroxidation mediated by oxygen radicals plays a crucial role in the pathogenesis of the gastric ulceration induced by the Fe/ASA solution.
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PMID:A new gastric ulcer model in rats produced by ferrous iron and ascorbic acid injection. 853 16


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