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Acetaldehyde dehydrogenase inhibition

Oxidation of acetaldehyde is inhibited by disulfiram, a drug that has been used to deter drinking by alcohol-dependent patients undergoing treatment. When ethanol is consumed in the presence of disulfiram, acetaldehyde accumulates and causes an unpleasant reaction of facial flushing, nausea, vomiting, dizziness, and headache. Several other drugs (eg, metronidazole, cefotetan, trimethoprim) inhibit aldehyde dehydrogenase and can cause a disulfiram-like reaction if combined with ethanol. [Pg.534]

Disulfiram is an aversive therapy that works by inhibiting acetaldehyde dehydrogenase. Interactions between disulfiram and alcohol can result in potentially severe reactions, such as myocardial infarction, congestive heart failure, respiratory depression and death. Patients taking disulfiram should be warned of the possible presence of alcohol in liquid medicines, tonics, foods and even in toiletries and mouthwashes. Patient adherence to disulfiram is poor and there is a lack of strong evidence for its effectiveness, thus it is not routinely recommended. [Pg.349]

Some aminocyclopropanes show biochemical activities. In some cases this is due to reactions of the three-membered ring (e.g. inhibition of acetaldehyde dehydrogenase by 4,... [Pg.1342]

Coprine (506) was isolated from the inky cap mushroom Coprinus atramentarius 416,613 mushroom proved to be non-toxic generally, but it caused severe illness when taken together with alcohol. It was found that semiaminal 4, the product of hydrolysis of 506, was the active substance inhibiting acetaldehyde dehydrogenase 61 -624... [Pg.1420]

Coprine (23), which has been isolated from the edible mushroom Coprinus atramentarius, yields 1-aminocyclopropanol upon digestion. This results in severe illness when consumed together with alcohol, because 1-aminocyclopropanol inhibits acetaldehyde dehydrogenase, resulting in accumulation of acetaldehyde in the blood. [Pg.1631]

Disulfiram inhibits acetaldehyde dehydrogenase, the enzyme that metabolizes alcohol it is not used for amphetamine abuse. [Pg.317]

C. Trichloroethylene or a metabolite may act to inhibit acetaldehyde dehydrogenase, blocking the metabolism of ethanol and causing degreaser s flush. ... [Pg.359]

Uncertain. It seems possible that furazolidone acts like disulfiram by inhibiting the activity of acetaldehyde dehydrogenase (see Alcohol + Disulfiram , p.61). [Pg.63]

It is thought that paraldehyde is depolymerised in the liver to acetaldehyde, and then oxidised by acetaldehyde dehydrogenase. Since disulfiram inhibits this enzyme, concurrent use would be expected to result in the accumulation of acetaldehyde and result in a modified disulfiram reaction. However, studies in animals given disulfiram and paraldehyde... [Pg.546]

Inhibits acetaldehyde dehydrogenase. Used to treat alcoholism. PisuHiram causes acetaldehyde (which has unpleasant effects) to accumulate... [Pg.66]

Figure 29.1 shows that acetaldehyde is metabolised in liver mitochondria by acetaldehyde dehydrogenase to form acetate and NAD forms NADH resulting in a high ratio of NADH NAD. This high ratio of NADH NAD prevents oxidation by the hydroxyacyl CoA dehydrogenase reaction, therefore p-oxidation is inhibited. [Pg.67]

Cocaine As weU as inhibiting acetaldehyde dehydrogenase, disulfiram inhibits dopamine beta-hydroxylase, increasing dopamine and reducing noradrenaline concentrations. [Pg.1016]

IPP, and/or DMAPP) can also cause sharp growth inhibition, which can be alleviated by the coexpression of a codon-optimized terpene synthase from the artemisinin pathway [27, 28]. Additionally, the production of lycopene was increased in E. coli by assembling a synthetic mevalonate pathway, which included mevalonate kinase and 5-diphosphomevalonate decarboxylase from yeast, human 5-phosphomevalonate kinase, and E. coli IPP/DMAPP isomerase [29]. Finally, studies on isoprenoid production in S. cerevisiae mainly focused on the mevalonate pathway. For example, Shiba et al. successfully amplified the flux to mevalonate in S. cerevisiae by overexpressing acetyl-CoA synthetase from Salmonella enterica and acetaldehyde dehydrogenase [30]. [Pg.481]

Ethanol is almost entirely metabolized in the liver. The first step, oxidation by alcohol dehydrogenase, yields acetaldehyde, a reactive and toxic compound. Essentially all of the acetaldehyde is converted to acetate by the liver enzyme aldehyde dehydrogenase. Aldehyde dehydrogenase is inhibited by the drag disulfiram. Given alone, disulfiram is a nontoxic substance. However, ethanol consumption in the presence of... [Pg.52]

The effect is mainly due to the inhibition of NAD+-dependent aldehyde dehydrogenase (ALDH) which causes an accumulation of acetaldehyde in the body after ethanol ingestion [17]. The compound responsible for the physiological activity of C. atramentarius is coprine 16, a AT -(l-hydroxycyclopropyl)-L-glutamic acid amide which has been isolated and synthesized, [16a,b]. Thus, when fed... [Pg.4]

Most of the human experience with disulfiram has come from its use as an avoidance therapy for alcoholism. Metabolites of disulfiram inhibit aldehyde dehydrogenase, resulting in elevated levels of acetaldehyde after ethanol ingestion. Side effects include flushing of the face, tachycardia, severe headache, apprehension, hyperpnea, hypotension, dizziness, nausea, vomiting, and fainting. Severe reactions may include convulsions, myocardial infarction, and marked respiratory depression. ... [Pg.287]

It exerts its action by inhibiting aldehyde dehydrogenase enz5une. Disulfiram thus increases the concentration of acetaldehyde in body when ethanol is ingested by an individual pretreated with disulfiram. The symptoms and signs produced... [Pg.397]

Disulfiram (Antabuse) inhibits aldehyde dehydrogenase irreversibly, causing an increase in the level of acetaldehyde, formed from ethanol by the enzyme alcohol dehydrogenase. This results in nausea, vomiting, and other symptoms in the human—hence its use as a deterrent in alcoholism. Inhibition by disulfiram appears to be irreversible, the level returning to normal only as a result of protein synthesis. [Pg.186]


See other pages where Acetaldehyde dehydrogenase inhibition is mentioned: [Pg.338]    [Pg.76]    [Pg.1421]    [Pg.2571]    [Pg.23]    [Pg.184]    [Pg.1818]    [Pg.282]    [Pg.28]    [Pg.130]    [Pg.45]    [Pg.61]    [Pg.68]    [Pg.151]    [Pg.248]    [Pg.212]    [Pg.212]    [Pg.165]    [Pg.278]    [Pg.922]    [Pg.848]    [Pg.709]    [Pg.67]    [Pg.1323]    [Pg.156]    [Pg.269]    [Pg.501]    [Pg.181]    [Pg.315]   
See also in sourсe #XX -- [ Pg.1342 , Pg.1420 , Pg.1421 ]




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