Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The organism frequently colonizing the stomach of patients suffering from chronic active gastritis and peptic ulcer disease--Helicobacter pylori--possesses marked alcohol dehydrogenase (ADH) activity. Consequently, Helicobacter infection may contribute to the capacity of the stomach to metabolize ethanol and lead to increased acetaldehyde production. To study this hypothesis, we first determined ADH activity in a variety of H. pylori strains originally isolated from human gastric mucosal biopsies. ADH activity was also measured in endoscopic gastric mucosal specimens obtained from H. pylori-positive and -negative patients. Furthermore, we used a mouse model of Helicobacter infection to determine whether infected animals exhibit more gastric ethanol metabolism than noninfected controls. Most of the 32 H. pylori strains studied possessed clear ADH activity and produced acetaldehyde. In humans, gastric ADH activity of corpus mucosa did not differ between H. pylori-positive and -negative subjects, whereas in antral biopsies ADH activity was significantly lower in infected patients. In mice, gastric ADH activity was similar or even lower in infected animals than in controls, depending on the duration of infection, despite the fact that the infectious agent used--Helicobacter felis--showed ADH activity in vitro. In accordance with this, Helicobacter infection tended to decrease rather than increase gastric ethanol metabolism in mice. In humans, it remains to be established whether the observed decrease in antral ADH activity associated with H. pylori infection can lead to reduced gastric first-pass metabolism of ethanol.
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PMID:Helicobacter infection and gastric ethanol metabolism. 769 20

Sex and age differences in gastric alcohol dehydrogenase activity in relation to abnormalities of gastric histology and Helicobacter pylori infection were determined in 63 patients (32 men and 31 women) undergoing upper endoscopy for gastrointestinal symptoms. No sex difference was found in gastric alcohol dehydrogenase activity. Males older than 50 years had lower enzyme activity than younger males. Patients with H. pylori and/or moderate to severe chronic and acute inflammation and epithelial mucin depletion had lower alcohol dehydrogenase activity in the antrum, but not in the fundus. H. pylori was found more frequently in the older male patients. Antral alcohol dehydrogenase was most decreased in older patients of both sexes with H. pylori infection. In conclusion, H. pylori infection and/or chronic active gastritis are important causes of low gastric alcohol dehydrogenase activity.
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PMID:Effects of Helicobacter pylori infection and gastritis on gastric alcohol dehydrogenase activity. 797 87

Traditional assays of alcohol dehydrogenase (ADH) activity in gastric mucosa use spectrophotometry of tissue homogenates, which are based on the reduction of nicotinamide adenine dinucleotide (NAD). We describe a colorimetric method using the coupled reduction of N,N-dimethyl-4-nitrosoaniline. This method has increased sensitivity, allowing activity to readily be determined in standard endoscopic biopsies. Tissue homogenisation has been replaced by an incubation stage, and the method has been optimised for a 96-well plate reader, allowing rapid processing of large numbers of samples. We found that Helicobacter pylori infection and age have a significant effect on gastric ADH activity.
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PMID:A sensitive, colorimetric, microtitre assay for alcohol dehydrogenase in standard endoscopic gastric biopsies. 1210 80

Bismuth compounds have been widely used for the treatment of ulcers and Helicobacter pylori infection, and enzyme inhibition was thought to be crucial for bismuth anti-microbial activity. We have investigated the interaction of colloidal bismuth subcitrate (CBS) with alcohol dehydrogenase and our results demonstrate that bismuth can effectively inhibit the enzyme. Kinetic analysis revealed that CBS acted as a non-competitive inhibitor of yeast alcohol dehydrogenase. Both UV-vis and fluorescence data show that interaction of CBS with the enzyme exhibits biphasic processes. Bismuth can replace only half of Zn(II) from the enzyme (i.e., about one Zn(II) per monomer). Surprisingly, binding of CBS also induces the enzyme dissociation from its native form, tetramer into dimers. The inhibition of Bi(III) on the enzyme is probably due to its direct interference with the zinc sites. This study is likely to provide an insight into the mechanism of action of bismuth drugs.
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PMID:Inhibition of alcohol dehydrogenase by bismuth. 1527 9

Human gastric mucosa contains three classes of alcohol dehydrogenase (ADH) isoenzymes: I, III, and IV. Various factors have been found to influence gastric ADH activity. One of them is Helicobacter pylori infection, which is associated with gastric mucosal injury and leads to a decrease in gastric ADH activity. The aim of the study was to assess the effect of H. pylori infection on the serum activity of ADH isoenzymes. Serum samples were taken from 35 patients with H. pylori infection and from 35 healthy subjects. For measurement of class I isoenzyme activity we employed the fluorometric method, with class-specific fluorogenic substrate (4-methoxy-1-naphthaldehyde). The activities of class III and IV ADH isoenzymes were measured by the photometric method with formaldehyde and with m-nitrobenzaldehyde as substrate, respectively. Total activity of ADH was measured by a photometric method with p-nitrosodimethylaniline. The total activities of ADH and class IV isoenzyme were significantly higher in sera of patients with H. pylori infection compared to healthy subjects. The serum activity of other tested isoenzymes of ADH did not differ significantly between infected and noninfected groups. We conclude that H. pylori infection of gastric mucosa is reflected in the serum by a significant increase in class IV and total ADH activity.
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PMID:Alcohol dehydrogenase (ADH) isoenzyme activity in the sera of patients with Helicobacter pylori infection. 1740 75

Endogenous intoxication indices, such as the levels of medium-weight molecules and oligopeptides, albumin binding ability, and the blood activity of NADH-alcohol dehydrogenase, were studied in 326 children with chronic gastroduodenitis and duodenal ulcerative disease, including 252 and 74 children with and without Helicobacter pylori infection, respectively. High endogenous intoxication was detected in the presence of Helicobacter pylori. The paper shows it possible to use the level of medium-weight molecules and oligopeptides, toxicity index, the blood activity of NADH-alcohol dehydrogenase as biochemical markers of the negative impact of Helicobacter pylori.
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PMID:[Characteristics of endogenous intoxication in children with Helicobacter pylori-associated gastroduodenal diseases]. 1880 8

Chronic gastritis is common in the alcoholic. It is characterized by histological inflammation of the gastric mucosa and is associated with variable symptomatology. Its etiology is still the subject of debate. Recently, a new alcohol dehydrogenase isoenzyme, called sigma ADH, absent from the liver but predominant in the upper GI tract, has been fully characterized, its gene cloned, and it appears to play a major role in gastric ethanol metabolism. Indeed, it has now been established, both in vivo in experimental animals and in vitro in cultured human gastric cells, that alcohol is metabolized in the gastric mucosa, resulting in the production of acetaldehyde, a toxic metabolite. In addition, Helicobacter pylori infection is common in the alcoholic, resulting in the breakdown of urea to ammonia, another toxic product. A number of studies carried out over the last 40 years revealed that antibiotic treatment eradicates ammonia production and results in histological and symptomatic improvement in the majority of patients with alcoholic gastritis. Non-invasive tests for the detection of H. pylori are now available which will facilitate the large scale studies needed to confirm whether, in H. pylori -positive patients, antibiotics should become routine treatment for alcoholic gastritis.
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PMID:Gastritis in the alcoholic: relationship to gastric alcohol metabolism and Helicobacter pylori. 2673 17