Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peptidases, phosphatases, glycosidases, non-specific esterases, succinate dehydrogenase, cholinesterases, and carbohydrate components were studied in bioptic material of the normal and diseased human stomach using well established older, modified older, and new qualitative histochemical methods. For the first time, an enzyme pattern is reported for all regions of the human mucosa. Local and regional enzyme histochemical differences existed between the cardiac, fundic, body, and pyloric mucosa. Differences were absent, however, in the same region, and no differences were found between the anterior and posterior wall and the large and small curvature of the stomach. In cases of histologically less severe gastritis as a rule, enzyme histochemical changes were not found. They were numerous, however, in biopsies of patients with severe gastritis; only amino-peptidases A and M were unchanged. Dipeptidyl peptidase IV was absent; gamma-glutamyl transpeptidase exhibited individual differences. Alkaline phosphatase occurred in the pericapillary stroma and adenosine phosphates were not hydrolysed in atrophic glandular epithelia. Activity increases of lysosomal dipeptidyl peptidase I and beta-D-glucuronidase were typical for inflammatory infiltration processes of the gastric mucosa. Severe atrophy was accompanied by an activity decrease of glandular non-specific esterases, dipeptidyl peptidase II, and beta-N-acetyl-D-glucosaminidase and an activity decrease of the stromal peptidases and glycosidases. Enzyme activity was absent in the gastric glands proper in cases of total atrophy. An increase in macrophage number was primarily linked with an increase in acid phosphatase activity. Alkaline phosphatase, aminopeptidase M and gamma-glutamyl transpeptidase activities were enhanced in malignant neoplasms. High activities of all peptidases and alkaline phosphatase were found in the brush border of surface epithelial cells in cases of intestinal metaplasia. Except for dipeptidyl peptidase I and II, the enzyme pattern corresponds to that of small intestinal enterocytes. Compared with histological routine procedures for gastric diagnosis and assessment of the course enzyme histochemical methods deliver additional information; practically, however, the enzyme histochemical analysis of gastric biopsies are only useful in special cases.
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PMID:[Histochemical studies of human stomach biopsies with special reference to hydrolases]. 313 86

Changes in levels of such redox enzymes of gastric mucosa as cytochrome oxidase, carboanhydrase and succinic dehydrogenase occurring in various forms of chronic gastritis were assessed with respect to morphological peculiarities and secretory function. A total of 102 cases (77--various forms of gastritis, 11--gastric neoplasms and 14--controls) were examined. Specific changes in atrophic antral and chronic histamine-resistant achlorhydric gastritis were identified.
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PMID:[Activity of various intracellular enzymes of the gastric mucosa in chronic gastritis and tumors]. 632 May 38

Gastric biopsies were performed before and after a 1-month aluminium phosphate gel treatment on 12 patients with gastritis or peptic ulcer requiring endoscopy. The sections were stained with various dyes used in histoenzymatic techniques, and colour intensity was evaluated double-blind by means of 0 to 5 scores. Compared with pretreatment levels, there was a statistically significant rise in PAS-toluidine blue activity, which measures mucus secretion (p less than 0.001) and in succinic dehydrogenase activity, an enzyme associated with cell respiration (p less than 0.05). The meaning of these changes is discussed. The mode of action of aluminum phosphate gels on the gastric mucosa remains hypothetical, but a direct contact induction mechanism seems more acceptable than an indirect mechanism involving non-specific reduction in intragastric acidity. Provided the results are statistically evaluated on a sufficient number of samples, PAS-toluidine blue and succinic dehydrogenase stains appear to constitute an easily measurable potential index of intracellular metabolic activity within the gastric mucosa. They could be used as markers to study the efficacy and biochemical mode of action of old and new drugs for gastro-duodenal disorders.
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PMID:[Histoenzymatic study of the effects of aluminium phosphate on the gastric mucosa (author's transl)]. 724 81

The pathophysiology of gastritis involves an imbalance between gastric acid attack and mucosal defence. In addition, the gastric mucosal injury results in adenosine triphosphate (ATP) depletion leading to mitochondrial dysfunction. Several studies have shown the association of mitochondrial disorders with gastrointestinal dysfunction. In the present study, we investigated the activity of mitochondrial respiratory chain complexes activity in the stomach of rats with gastritis induced by indomethacin (IDM) and treated with omeprazole (OM), N-acetylcysteine (NAC) and the gastrin-releasing peptide receptor (GRPR) antagonist RC-3095. Adult male Wistar rats were pre-treated for 7 days with OM, NAC, RC-3095, combination of OM plus RC-3095, OM plus NAC and water (control). The animals were then submitted to fasting for 24 hr; IDM was administered. The rats were killed 6 hr later, and the stomachs were used for evaluation of macroscopic damage and respiratory chain activity. Our results showed that complex I and IV activities were not affected by administration of IDM. On the other hand, complex II and III activities were inhibited. In addition, OM plus RC-3095 and OM plus NAC did not reverse complex II activity inhibition. However, the complex III activity inhibition was reversed only with the combined use of OM plus RC-3095 and OM plus NAC. Our results are in agreement with previous studies indicating mitochondrial dysfunction in the pathophysiology of gastrointestinal tract disease and we suggest that GRPR antagonism might be a novel therapeutic strategy in gastritis.
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PMID:Gastrin-releasing peptide receptor antagonist or N-acetylcysteine combined with omeprazol protect against mitochondrial complex II inhibition in a rat model of gastritis. 2113 29

Switching of cellular energy production from oxidative phosphorylation (OXPHOS) by mitochondria to aerobic glycolysis occurs in many types of tumors. However, the significance of this switching for the development of gastric carcinoma and what connection it may have to Helicobacter pylori infection of the gut, a primary cause of gastric cancer, are poorly understood. Therefore, we investigated the expression of OXPHOS complexes in two types of human gastric carcinomas ("intestinal" and "diffuse"), bacterial gastritis with and without metaplasia, and chemically induced gastritis by using immunohistochemistry. Furthermore, we analyzed the effect of HP infection on several key mitochondrial proteins. Complex I expression was significantly reduced in intestinal type (but not diffuse) gastric carcinomas compared to adjacent control tissue, and the reduction was independent of HP infection. Significantly, higher complex I and complex II expression was present in large tumors. Furthermore, higher complex II and complex III protein levels were also obvious in grade 3 versus grade 2. No differences of OXPHOS complexes and markers of mitochondrial biogenesis were found between bacterially caused and chemically induced gastritis. Thus, intestinal gastric carcinomas, but not precancerous stages, are frequently characterized by loss of complex I, and this pathophysiology occurs independently of HP infection.
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PMID:Oxidative Phosphorylation System in Gastric Carcinomas and Gastritis. 2874 36