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 regulation of ornithine decarboxylase activity was studied in freshly isolated rat hepatocytes incubated in a chemically defined medium for 5 h. Glucagon, dibutyryl cyclic AMP, insulin and dexamethasone produced dramatic increases in ornithine decarboxylase activity, 6--100-times the basal activity. Actinomycin D inhibited completely the stimulatory action of these substances. With glucagon, dibutyryl cyclic AMP and insulin, the rise in ornithine decarboxylase activity was rapid but transient, peaking at 200 min and then declining rapidly. By contrast, the response to dexamethasone was gradual and sustained in the 5 h incubation. The transient nature of the response to glucagon was unaltered by repeated additions of optimally effective doses of glucagon suggesting the development of 'refractoriness' to the actions of this hormone. Ethanol oxidation inhibited by 50% the stimulation of ornithine decarboxylase by glucagon and dexamethasone and this effect was blocked by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Acetate (2.5--20 mM), the metabolic product of hepatic ethanol oxidation, was also effective. The data indicate that glucagon, insulin and glucocorticoids are all effective in stimulating the activity of ornithine decarboxylase in isolated hepatocytes but they differ in their duration and time of peak of action. Additionally, the inhibitory effect of ethanol on the hormonal stimulation of ornithine decarboxylase is dependent on its oxidation and may be mediated by acetate.
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PMID:Hormonal control of ornithine decarboxylase in isolated liver cells and the effect of ethanol oxidation. 22 51

Suicide inhibitors of acetylenic structure can inactive many enzymes playing an important role in the cancer cell metabolism. This type of inhibitors presents a fantastic interest because of its original inhibition mode: it is the catalytic mechanism of the enzyme itself which make the inhibitor reactive. In this way, thymidylate synthetase, ornithine decarboxylase, aldehyde dehydrogenase, aldehyde reductase are inhibit by acetylenic substrates. These very efficient compounds will allow to envisage a more selective chemotherapy of cancer.
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PMID:[Acetylenic enzyme inhibitors: their role in anticancer chemotherapy]. 228 2

Male rat liver undergoes a process of demasculinization during hepatic regeneration following partial hepatectomy. The possibility that antiandrogens might potentiate this demasculinization process and in so doing augment the hepatic regenerative response was investigated. Adult male Wistar rats were treated with the antiandrogen flutamide (2 mg/rat/day or 5 mg/rat/day subcutaneously) or vehicle for three days prior to and daily after a 70% partial hepatectomy. At various times after hepatectomy, the liver remnants were removed and weighed. Rates of DNA and polyamine synthesis were assessed by measuring thymidine kinase and ornithine decarboxylase activities, respectively. Hepatic estrogen receptor status and the activity of alcohol dehydrogenase, an androgen-sensitive protein, were measured. Prior to surgery, the administration of 5 mg/day flutamide reduced the hepatic cytosolic androgen receptor activity by 98% and hepatic cytosolic estrogen receptor content by 92% compared to that present in vehicle-treated controls. After hepatectomy, however, all differences in sex hormone receptor activity between the treatment groups were abolished. The rate of liver growth after partial hepatectomy in the three groups was identical. Moreover, hepatectomy-induced increases in ornithine decarboxylase activity and thymidine kinase activity were comparable. These data demonstrate that, although flutamide administration initially alters the sex hormone receptor status of the liver, these affects have no effect on the hepatic regenerative response following a partial hepatectomy.
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PMID:Effect of antiandrogen flutamide on measures of hepatic regeneration in rats. 259 58

Intragastric administration of ethanol greatly inhibited ovarian ornithine decarboxylase (L-ornithine carboxy-lyase EC 4.1.1.17) stimulated by human chorionic gonadotropin in vivo. The inhibition occurred only if the treatment with ethanol was started before the injection of hormone. The use of inhibitors for alcohol dehydrogenase and aldehyde dehydrogenase clearly showed that the observed inhibition was a direct effect of ethanol itself. When rat ovarian cells were incubated in vitro with human chorionic gonadotropin the activity of ornithine decarboxylase was also markedly stimulated. This stimulation could also be inhibited by ethanol. Moreover, actinomycin D and alpha-amanitin inhibited the stimulation of ornithine decarboxylase, showing that the enhanced activity in vitro resulted from the synthesis of new mRNA for ornithine decarboxylase. The time dependence of the inhibition caused by ethanol addition resembled that after addition of actinomycin D. This supports the view that one site where ethanol inhibits protein synthesis is at the transcriptional level.
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PMID:Inhibition of rat ovarian ornithine decarboxylase by ethanol in vivo and in vitro. 724 3

Eleven rat genes have been assigned to rat chromosomes by use of mouse x rat somatic hybrids and/or use of linkage to known chromosome markers. Among them, the genes for the inducible nitric oxide synthase (Nos2) and for a vasoactive intestinal peptide receptor (Vipr) are potential candidates for genetic regulation of blood pressure and were localized to rat Chromosomes (Chrs) 10 and 8 respectively. Genes for gastric H,K-ATPase alpha subunit (Atp4a), Class I alcohol dehydrogenase (Adh), and aldolase C (Aldoc) were localized to Chrs 1, 2, and 10 respectively, and thus provide more DNA markers for genetic mapping of quantitative trait loci for blood pressure on those chromosomes. Genes for alkaline phosphatase (Alp1) and cardiac AE-3 Cl-/HCO3- exchanger (Ae3) were both localized to Chr 9. Genes for glutamate dehydrogenase (Glud) and gastric H,K-ATPase beta subunit (Atp4b) were localized to Chr 16. The ornithine decarboxylase (Odc) gene and ornithine decarboxylase pseudogene (Odcp) were localized to Chrs 6 and 11 respectively.
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PMID:Chromosomal assignment of 11 loci in the rat by mouse-rat somatic hybrids and linkage. 787 82