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Generic Antabuse is a high-quality medication which is taken in treatment of alcoholism. Generic Antabuse acts by blocking the breakdown of alcohol, causing unpleasant side effects (eg, vomiting, upset stomach) when even a small amount of alcohol is consumed. It is an alcohol-abuse deterrent.

Other names for this medication:
Alcophobin, Anticol, Aversan, Diabuse, Disulfiramo, Disulfiramum, Disulphiram, Esperal, Etabus, Etiltox, Refusal, Tenutex

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Also known as:  Disulfiram.


Generic Antabuse is a perfect remedy in struggle against alcoholism.

Generic Antabuse acts by blocking the breakdown of alcohol, causing unpleasant side effects (eg, vomiting, upset stomach) when even a small amount of alcohol is consumed. It is an alcohol-abuse deterrent.

Antabuse is also known as Disulfiram, Antabus.

Generic name of Generic Antabuse is Disulfiram.

Brand name of Generic Antabuse is Antabuse.


Do not take the first dose of Generic Antabuse for at least 12 hours after drinking alcohol.

Take Generic Antabuse orally with or without food.

If you want to achieve most effective results do not stop taking Generic Antabuse suddenly.


If you overdose Generic Antabuse and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep in a tight light resistant container. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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The most common side effects associated with Antabuse are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Antabuse if you are allergic to Generic Antabuse components.

Do not take Generic Antabuse if you are pregnant, planning to become pregnant, or are breast-feeding.

Notify your doctor immediately if you experience yellowing of the skin or eyes, dark urine, weakness, tiredness, loss of appetite, or nausea and vomiting. These may be signs of a liver problem.

Before you have any medical or dental treatments, emergency care, or surgery, tell the health care provider or dentist that you are using Generic Antabuse.

Use Generic Antabuse with extreme caution in children.

Avoid all alcohol including alcohol found in sauces, vinegar, mouthwash, liquid medicines, lotions, after shave, or backrub products.

Avoid machine driving.

It can be dangerous to stop Generic Antabuse taking suddenly.

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A review is made of the pharmacological, biochemical and chemical aspects of the unpleasant 'Antabuse-like' reaction that may be induced in drinkers of alcohol by pre-treatment with certain beta-lactam antibiotics with a 1-methyltetrazole-5-thiol sidechain (such as moxalactam, cefamandole and cefoperazone). The symptoms are due to abnormally elevated blood acetaldehyde levels consequent upon the inactivation of hepatic aldehyde dehydrogenase. There is very little direct effect of the antibiotics on this enzyme and therefore it is concluded that a reactive metabolite of the antibiotics' essential sidechain is responsible for the reaction. A likely candidate for this active species is either the symmetrical disulphide 5,5'-dithiobis(1-methyltetrazole) formed by oxidation of 1-methyltetrazole-5-thiol, or the related mixed disulphide, methyl 5-(1-methyltetrazolyl) disulphide. The first of these is a potent inactivator of cytoplasmic aldehyde dehydrogenase only, the second affects both cytoplasmic and mitochondrial isoenzymes. 1-Methyltetrazole-5-thiol or derivatives have the potential to be used therapeutically as 'anti-alcohol' compounds in the same way as disulfiram (Antabuse) or calcium cyanamide.

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Several studies have reported that hydrogen peroxide (H2O2) is related to the toxicity of amyloid β (Aβ), and that the accumulation of Aβ in the lenses of humans causes lens opacification. In this study, we investigate the accumulation of Aβ1-42 in the lenses of UPL rats, which then leads to lens opacification. In addition, we demonstrate the effect of disulfiram eye drops (DSF), a potent radical scavenger, on Aβ1-42 accumulation in the lenses of UPL rats. The H2O2 levels in 46- to 60-day-old UPL rat lenses are significantly higher than in normal rats, and the Aβ1-42 levels in 53- and 60-day-old UPL rats are also increased only in lens epithelium containing capsules (capsule-epithelium), not in the lens cortex and nucleus. However, no increases in amyloid precursor protein (APP), β- or γ-secretase mRNA were observed in lenses of the corresponding ages. It has been thought that Aβ1-42 that accumulates in the lenses of UPL rats is actually produced in another tissue containing neuronal cells, such as brain or retina. Aβ1-42 levels in the brain and retina rise with aging, and the levels of APP, β- and γ-secretase mRNA in the retinas of 53-day-old UPL rats with opaque lenses are significantly higher than in 25-day-old UPL rats with transparent lenses. In contrast to the results in retinas, the levels of APP, β- and γ-secretase mRNA in the brains of 25- and 53-day-old UPL rats are similar. On the other hand, in an in vitro study, Aβ1-42 attachment in the lens capsule-epithelium of UPL rats was found to increase in H2O2. In addition, in an in vivo study, the inhibition of H2O2 by DSF was found to attenuate the increase in Aβ1-42 in the lens capsule-epithelium of 60-day-old UPL rats. Taken together, we hypothesize that excessive H2O2 in the lens enhances the attachment of Aβ1-42 in the lens capsule-epithelium of UPL rats, and that the instillation of DSF has the ability to attenuate the attachment of Aβ1-42 by inhibiting H2O2 production in lens. These findings provide significant information that can be used to design further studies aimed at developing anti-cataract drugs.

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The authors measured plasma levels of norepinephrine (NE) and dopamine beta-hydroxylase (DBH), pulse rates, and blood pressures of 81 hospitalized alcoholic patients. Treatment with 500 mg/day of disulfiram (but not 250 mg/day or placebo) resulted in small but significant increases in plasma NE and in blood pressure. The 500-mg dose did not appreciably inhibit DBH. Patients receiving high doses of disulfiram should have their blood pressure monitored and their dose decreased to 250 mg/day when possible.

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The present experiment examined effects of disulfiram (Antabuse) administration on behavioral measures of nociception (hot plate and tail flick), peripheral muscular performance (grip strength), motivated performance, balance, and coordination (rotorod) in 24 male Sprague-Dawley rats during and 2 wk after an eight-day administration of disulfiram. In addition, peptidylglycine 5(-hydroxylating monooxygenase (PHM) activity in several tissues and levels of alpha-amidated alpha-melanocyte stimulating hormone (alpha-MSH) in the neurointermediate lobe of the pituitary were assayed to evaluate biochemical effects of disulfiram. These particular assays were included because it has been reported that disulfiram affects alpha-amidated peptides via alteration of PHM activity. Decrements in all behavioral measures, except tail flick, occurred after one week of disulfiram administration. Decrements in grip strength continued for the 2 wk after cessation of disulfiram. Dose-related reductions in changes in PHM activity and levels of alpha-MSH were found 2 wk after cessation of disulfiram administration. The time course of the results suggest that changes in PHM activity may underlie decrements in grip strength. The present experiment provides a paradigm for further investigations of effects of alpha-amidated peptides on behavior.

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Despite the availability of currently approved medications and various psychosocial therapies, alcohol abuse and dependence are increasingly prevalent in the United States, and carry a significant socioeconomic burden. Recently, the novel anti-epileptic topiramate has shown great promise as a new treatment for this disorder. The objective of this review is to discuss the limitations of the currently available options for treating alcohol dependence, to review the results of clinical trials assessing the efficacy of topiramate in treating alcohol dependence, and to describe the pharmacological characteristics and mechanisms of action of topiramate as related to this indication. We systematically reviewed Medline, EMBASE, Cochran Reviews and PsycINFO search terms included combinations of the terms "pharmacotherapy" "topiramate", "alcoholism" and "alcohol dependence." Searches were last updated 24 October 2008. Currently approved treatments include disulfiram, naltrexone tablets and injection, and acamprosate. Of these, naltrexone has shown the most benefit, however the effect size is small and may reach its most promising potential when combined with medical management. Alternatively, through multiple mechanisms of action, topiramate in clinical trials has demonstrated safety and efficacy in decreasing both craving and withdrawal symptoms and increasing quality of life measures among alcohol-dependent individuals. The findings of this review suggest that topiramate is a promising new option for the treatment of alcohol dependence, and may offer substantial benefits over currently approved medications. While the manufacturer will not pursue approval of an indication for the treatment of alcohol dependence, the drug will soon be available generically, making it more affordable for a greater proportion of the public.

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This paper is a brief review which deals with research findings, clinical issues, and strategies in the pharmacotherapy of alcoholism. The pharmacotherapy is presented according to different clinical phases of the alcoholic process. The acute intoxicated patient receives supportive treatment, to be clinically observed to prevent severe respiratory depression, aspiration of vomitus, and severe alcohol withdrawal syndrome. Benzodiazepine therapy is the mainstay in treating alcohol withdrawal syndrome. Disulfiram is the only chemical used in the United States to deter the alcoholic patient from further alcohol drinking. Although there is not a specific agent for alcoholism per se during the sobriety state, the alcoholic patients' concurrent underlying psychiatric conditions (such as schizophrenia, anxiety, and depression) should be treated properly and adequately.

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Two enzymatic reactions, catalyzed by mouse lung microsomes and distinguishable by selective inhibition and kinetic studies, lead to irreversible binding of benzo[a]pyrene to macromolecules present in vitro reaction systems. One type (low Km) is inducible in the lungs of mice by treatment with benz[a]anthracene and is subject to inhibition by 7,8-benzoflavone. The other type (high Km) is predominant in lungs of untreated mice, but a small amount of low-Km activity is also present. The high-Km activity may be involved in carcinogenesis by benzo[a]pyrene, for it is inhibited by butylated hydroxytoluene, retinol or disulfiram, each of which is reported to have anticarcinogenic activity in intact animals.

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Patients with hazardous alcohol intake are overrepresented in emergency departments and surgical wards. These patients have an increased risk of postoperative complications with prolonged hospital stays and admissions to intensive care unit after surgery. In elective surgery, preoperative alcohol cessation interventions can reduce postoperative complications, but no studies have investigated the effect of alcohol cessation intervention at the time of acute fracture surgery. This protocol describes a randomised clinical trial that aims to evaluate the effect of a new gold standard programme for alcohol cessation intervention in the perioperative period regarding postoperative complications, alcohol intake and cost-effectiveness.

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The article discusses therapeutic potential of placebo and nocebo effects in treatment of substance use disorders. The authors review the background of the issue, describe neurobiological and psychological mechanisms of placebo effects and demonstrate their impact on psychotherapy of patients with substance use disorders. Attention is drawn to the clinical and ethical issues of practical use of placebo effects including that in terms of placebo-therapy, indirect suggestion psychotherapy, motivational interventions and cognitive-behavioral psychotherapy, psychotherapy with the use of disulfiram, psychopharmacotherapy with opioid antagonists. The authors conclude that the ethical use of placebo-effects in treatment of substance use disorders may improve its overall efficiency.

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The oral hypoglycemic agents, chlorpropamide (CP) and tolbutamide (TB) are known to elicit a clinical disulfiram-ethanol reaction (DER) when consumed with alcohol. In rats, this DER is manifested in vivo by the elevation of blood acetaldehyde (AcH) levels, a consequence of the inhibition of hepatic aldehyde dehydrogenase (AIDH). Administration of CP or TB to rats (1.0 mmol/kg, IP), followed by ethanol one hour before sacrifice, raised blood AcH levels 12- and 2-times that of control animals, respectively for CP and TB when measured at 3 hours, and 20-fold and 8-fold at 16 hours post drug administration. CP and TB had no effect on AIDH activity when incubated with either intact or osmotically disrupted rat liver mitochondria, indicating that a metabolite of CP or TB is responsible for the inhibition of AIDH in vivo. Hydrolysis products of CP, the 2'-hydroxylated products of CP, tolpropamide and tolethamide, or the 3'-hydroxylated analogs of CP and tolpropamide, were uniformly inactive in elevating ethanol-derived blood AcH. Pretreatment of rats with 3-amino-1,2,4-triazole or SKF-525A had no effect on the elevation of blood AcH mediated by CP or TB, while phenobarbital pretreatment decreased blood AcH by 69%. Although our results clearly indicated that side chain hydroxylation and subsequent oxidation do not play a role in AIDH inhibition by CP or TB, the nature of the side chain attached to the sulfonylurea moiety appears to influence this inhibitory activity in vivo. Thus, the order of activity in the homologous series was, chlorpropamide greater than chlorbutamide greater than chlorethamide much greater than chlormethamide, chlorisopropamide = 0.

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Two new products from the incubation of beta-carotene with intestinal mucosa homogenates of human, monkey, ferret, and rat were isolated using high-performance liquid chromatography (HPLC). Identification by comparing retention times in HPLC, by monitoring ultraviolet/visible spectra, by reduction to corresponding alcohol, by oxime formation, and by mass spectrometry demonstrated that they are beta-apo-13-carotenone and beta-apo-14'-carotenal. These compounds were not found in incubations done without intestinal homogenates or with disulfiram as an inhibitor. Under standard incubation conditions, these products increased linearly for 60 min and up to a protein concentration of 1.5 mg/mL and increased along with increasing concentrations of beta-carotene. Therefore, they are enzymatic cleavage products from beta-carotene. The formation of the beta-apo-13-carotenone and beta-apo-14'-carotenal provides direct evidence for an enzymatic excentric cleavage mechanism.

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In vitro studies suggest that the oxidation of quinidine to 3-hydroxyquinidine is a specific marker reaction for CYP3A4 activity. To assess the possible use of this reaction as an in vivo marker of CYP3A4 activity, we studied the involvement of cytochromes CYP2C9, CYP2E1 and CYP3A4 in the in vivo oxidative metabolism of quinidine.

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Since Chevens' report, in the early 50's that his patients under treatment Flomax Generic Dosage with the aldehyde dehydrogenase inhibitor, antabuse, could experience beneficial effects when drinking small volumes of alcoholic beverages, the role of acetaldehyde (ACD) in the effects of ethanol has been thoroughly investigated on pre-clinical grounds. Thus, after more than 25 years of intense research, a large number of studies have been published on the motivational properties of ACD itself as well as on the role that ethanol-derived ACD plays in the effects of ethanol. Accordingly, in particular with respect to the motivational properties of ethanol, these studies were developed following two main strategies: on one hand, were aimed to challenge the suggestion that also ACD may exert motivational properties on its own, while, on the other, with the aid of enzymatic manipulations or ACD inactivation, were aimed to test the hypothesis that ethanol-derived ACD might have a role in ethanol motivational effects. Furthermore, recent evidence significantly contributed to highlight, as possible mechanisms of action of ACD, its ability to commit either dopaminergic and opioidergic transmission as well as to activate the Extracellular signal Regulated Kinase cascade transduction pathway in reward-related brain structures. In conclusion, and despite the observation that ACD seems also to have inherited the elusive nature of its parent compound, the behavioral and biochemical evidence reviewed points to ACD as a neuroactive molecule able, on its own and as ethanol metabolite, to exert motivational effects.

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FSS was assessed cross-sectionally in 46 severe alcohol-dependent Biaxin 800 Mg patients participating in a close-meshed biopsychosocial treatment program. The FSS was measured with the Medical Outcome Study Social Support Survey.

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Very few cases of peripheral neuropathy as a complication of disulfiram therapy have been described. The clinical and electrodiagnostic features of two patients who developed a severe peripheral neuropathy during disulfiram administration are reported Geodon 4 Mg . Evidence is presented which suggests that disulfiram causes a dying-back axonal neuropathy.

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The effect of the scavenger compound disulfiram (Antabus) on postischemic cell injury was investigated. Rats were subjected to 90 min of liver ischemia and 3 h of reperfusion. The Aricept Generic Name extent of cell injury was evaluated morphologically by a dye exclusion test and a histochemical stain for calcium. It was found that pretreatment with disulfiram significantly reduced the number of injured cells compared to untreated controls.

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Previous research has identified a strong association between posttraumatic stress disorder (PTSD) and substance use disorder (SUD), necessitating the development of treatments that address both conditions. Some pharmacotherapies are effective for the treatment of PTSD and SUD alone, however; no medications have been proven to be effective for the combination of these conditions. We review the recent advances in pharmacological treatment of comorbid Zyrtec Weight Dosage PTSD and SUD. A randomized clinical trial of sertraline, a serotonin reuptake inhibitor (SSRI), did not show overall efficacy for comorbid PTSD and alcohol dependence (AD), although it may have efficacy among light drinkers. Another clinical trial demonstrated the efficacy of both disulfiram and naltrexone for the treatment of AD in individuals with PTSD. A more recent clinical trial suggested that norepinephrine uptake inhibitors may also have efficacy for the treatment of comorbid PTSD and AD. In animal and preliminary human studies, brain norepinephrine and glutamate/GABA have emerged as potential treatment targets for comorbid PTSD and SUD. Noradrenergic medications that are promising for comorbid PTSD and SUD include prazosin, guanfacine, and atomoxetine. Promising glutamate/GABA medications include topiramate, memantine, acamprosate, N-acetylcysteine (NAC), and ketamine. The safety and efficacy of these medications for the treatment of PTSD and SUD need to be tested in controlled clinical trials.

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Disulfiram is widely used in the treatment of chronic alcoholism. Adverse drug reactions with fatal outcome following disulfiram therapy are infrequent, and hepatic failure accounts for most of them. Since disulfiram is a cytochrome P450 (CYP450) enzyme system inhibitor, numerous interactions with several drugs metabolized in the liver have been reported. Like disulfiram, clarithromycin inhibits a CYP450 isoenzyme, but, despite its widespread use for the treatment of respiratory tract infections, no interactions with Dallas Botox Cheap disulfiram have been described as yet. We report a case of fatal toxic epidermal necrolysis (Lyell disease) and fulminant hepatitis shortly after starting treatment with clarithromycin in a patient who was receiving disulfiram. This is the first case of such a severe dermatosis in a patient receiving either disulfiram or clarithromycin therapy. The temporal relationship between drug administration and clinical symptoms in this case suggests a probable interaction between the 2 drugs.

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Short exposure (1-2 h) of cultured cells, derived from a transplantable murine mammary carcinoma, to sodium arsenite, 2,4-dinitrophenol (DNP), carbonylcyanide-3-chlorophenylhydrazone (CCP) or disulfiram, induced resistance to a subsequent heat treatment, similar to heat-induced thermotolerance. Optimum resistance to a test heat treatment of 45 min at 45 degrees C after sodium arsenite exposure was obtained at a concentration of 300 microM, after DNP exposure at 3mM, after CCP at 300 microM and after disulfiram exposure in the range 1-30 microM. Exposure of cells to CCP Losartan Cozaar Reviews , sodium arsenite or disulfiram led to enhanced synthesis of some proteins with the same molecular weight as 'heat shock' proteins. The pattern of enhanced synthesis of these proteins was agent specific. We could not detect significantly enhanced synthesis of the proteins after DNP using one-dimensional gel electrophoresis. These results suggest that enhanced stress protein synthesis is not a prerequisite for the development of thermal resistance.

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Treatment with disulfiram (DSF, 1000 mg/kg p.o.) 2 or 6 h prior to Coreg Dose s.c. injection of cyclophosphamide (CP) raised the acute toxicity of CP in male Sprague-Dawley rats by 60%. The acute LD50 was reduced from 236 mg/kg after application of CP alone to 90 mg/kg and 95 mg/kg after pretreatment with DSF 2 and 6 h prior to CP administration, respectively.

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Direct administration of acetaldehyde (100 mg/kg) had an anxiogenic effect at Avapro Side Effects User Reviews 1, 11 or 26 min after IP administration. Acetaldehyde was ten times more potent than ethanol at inducing corticosterone release. Disulfiram did not affect behavior on its own, but blocked the anxiolytic effect of ethanol at doses of 30 and 60 mg/kg, and had an anxiogenic effect at the highest dose (90 mg/kg) when co-administered with ethanol. Acetate did not affect any of the anxiety parameters.

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The results of the present study demonstrate that 1-aminobenzotriazole, a potent inhibitor of various CYP enzymes, seems to be the best candidate suitable for utilization in studies evaluating participation of CYP enzymes in metabolism of xenobiotics in various complex biological materials containing both CYP and peroxidase enzymes. Moreover, precaution to prevent misinterpretation of results is necessary in Biaxin And Alcohol cases when proadifen SKF525A, piperonylbutoxide, diethyldithiocarbamate, ketoconazole, α-naphtoflavone and ellipticine are used in similar studies (as CYP inhibitors in various complex biological materials containing both CYP and peroxidase enzymes), since these chemicals can except of CYP enzymes inhibit also peroxidase-mediated reactions.