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)

In 51 patients with gastric adenocarcinoma the fasting blood concentrations of hCG, beta hCG, alpha subunits, ADH, calcitonin, enteroglucagon, gastrin, GH, melatonin, somatostatin, estradiol, CEA and pepsinogen I in the peripheral vein were estimated by radioimmunoassay at the time of diagnosis and, in those who underwent surgery, 7 days after the operation, to determine the incidence of the modifications of the above mentioned substances' blood levels and the existence of possible markers. In presence of increases of the examined parameters greater than 50%, considering M +/- 2 SD of 10 control subjects as normal range, the tumours were examined immunohistochemically. In patients with gastric adenocarcinoma, in comparison with normal subjects, we found significant higher blood levels of hCG alpha subunits, gastrin and CEA and lower of melatonin, pepsinogen I and GH. The immunohistological results demonstrated CEA in both examined cases, alpha subunits in 2 of 6 (respectively in dysplasic areas and in surrounding non neoplastic mucosa) and enteroglucagon in 1 of 3 (dysplasic areas). Our results indicate that none of the parameters we examined, because of their non-specificity or of the low incidence of their modifications, can be considered a marker of gastric adenocarcinoma.
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PMID:[Changes in hormonal and biochemical parameters in gastric adenocarcinoma]. 180 10

The involvement of gastric mucosal metabolism of ethanol in ethanol-induced mucosal damage was studied in urethane anaesthetised rats. Pyrazole, an inhibitor of alcohol dehydrogenase (ADH), slightly aggravated the mucosal lesions produced by intragastric instillation of 30% (v/v) ethanol, but had no effect on increased mucosal permeability to ions, pepsinogen and fluid output or on gastric mucosal blood flow associated with mucosal injury. Induction of ADH by ethanol pre-treatment had no effect on the above-mentioned parameters. Intragastric instillation of acetaldehyde, the product of ethanol oxidation, did not cause lesions in the gastric mucosa. The results suggest that the gastric mucosal toxicity of ethanol may not be related to its metabolism in the gastric mucosa.
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PMID:Gastric mucosal oxidation of ethanol is not involved in ethanol-induced mucosal damage. 716 79