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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.

Side effects

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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Doctors of many specialties, including the family doctors, encounter the problems of alcohol abuse in their patients. Due to the fact that many symptoms of dangerous diseases can be masked by the fact of alcoholism, a brief doctor's visit has to be conducted with watchfulness, caution and care. Family doctors have some brief testes (such as CAGE test, AUDIT test), besides of precise anamnesis and blood chemistry, which make it easier to identify a patient with an alcohol problem. People with disabilities are more exposed to alcohol abuse since they often experience additional factors such as unemployment, social isolation and homelessness. All of the above factors foster the more frequent alcohol usage. In Poland the main treatment method of alcohol addiction is psychotherapy practiced in the rehab centers. The detoxification treatment is voluntary and free of charge even though the patients checking into those facilities are doing it against their will. They are forced to do so by entourage, family, spouse or risk of unemployment. Acamprozate is considered as a drug, run to extend abstaining from alcohol. In the past, therapy with disulfiram substance was common, but now, it is considered as unethical behaviour. In practice of medicine, a patient with alcohol addiction creates not onlya medical but also legal problems. Therefore keeping of detailed medical documentation is very important as it may become significant evidence in the future.

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CM enhances outcomes for CBT treatment of cocaine dependence, but disulfiram provided no added benefit to the combination of CM and CBT.

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Fifty-nine couples with an alcoholic husband, after receiving weekly BMT couples sessions for 5-6 months, were assigned randomly to get or not get 15 additional couples relapse prevention (RP) sessions over the next 12 months. Outcome measures were collected before and after BMT and at quarterly intervals for the 30 months after BMT.

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Individual therapists in office practice are often considered to have limited effectiveness in treating alcohol and drug dependence. In this article the author describes network therapy, an approach developed to assure greater success in such treatment. It uses psychodynamic and behavioral therapy while engaging the patient in a support network composed of family members and peers. A cognitive-behavioral model of addiction, based on the role of conditioned withdrawal in relapse, is described. Related techniques for securing abstinence are then reviewed; they augment individual psychotherapy to help patients avoid relapse caused by the affective and environmental cues that precipitate drug seeking. The role of social cohesiveness as a vehicle for engaging patients in treatment is outlined next, along with a related technique for enhancing an addicted patient's commitment to the therapy. This is done by using the patient's family and peers as a therapeutic network to join the patient at intervals in therapy sessions. The network is managed by the therapist to provide cohesiveness and support, undermine denial, and promote compliance with treatment. The author presents applications of the network technique designed to sustain abstinence and describes means of stabilizing members' involvement. Applications of network therapy to ambulatory detoxification, disulfiram and naltrexone administration, relapse prevention, and contingency contracting are reviewed.

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Cancer stem cells may be responsible for acquired pan-chemoresistance. As a drug used in clinic, DS may be repurposed as a CSC inhibitor to reverse the acquired pan-chemoresistance.

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Hepatic enzymes connected with the formation and metabolism of free D-glucuronic acid were affected in rats after treatment with disulfiram or diethyldithiocarbamate (300 mg/kg, intragastrically, per day, 4 X). The activities of UDPglucose dehydrogenase, UDPglucuronic acid pyrophosphatase, UDPglucuronosyltransferase and L-gulonate dehydrogenase were enhanced, while those of glucose-6-phosphate dehydrogenase, beta-glucuronidase and D-glucuronolactone dehydrogenase were inhibited. These changes were more pronounced with disulfiram than diethyldithiocarbamate. Treatment with phenobarbital (80 mg/kg, i.p., per day, 4 X) enhanced UDP glucuronosyl-transferase, but brought about different effects on the other enzymes. Concurrent administration of phenobarbital with disulfiram or diethyldithiocarbamate led to potentiation or antagonism of the primary effects of each compound when given alone. The results suggest that activation of the D-glucuronic acid pathway may proceed in various ways, and that it is not necessarily followed by a simultaneous induction of the microsomal mixed-function oxygenase activity.

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Acamprosate, disulfiram (DIS), naltrexone and nalmefene can be used in treating alcohol use disorders. The drugs are, however, underutilized.

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Alcohol--orally given in concentrations from 1 to 4 g/kg body-weight--leads to a reduction of mast cells in the guinea pig lung. At the same time a minor decrease of histamine concentration was observed. The incompatibility reaction with alcohol after disulfiram intake (DAR) shows an additional degranulation oft mast cells of the lungs and decrease of histamine-content. So far, there seems little difference between the influence of disulfiram alone and the DAR. Besides thrombocytes and basophile leucocytes, the mast cells of the lung are responsible for the release of histamine and serotonine during higher alcohol concentrations and alcohol-disulfiram-reactions. We think that the intolerance phenomena of humans after alcohol--f.e. in form of flush-reaction--is at least partly related to the concomitant influence oft mast cell-substances.

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Benzo[a]pyrene (BP) administered to female outbred ICR/Ha mice by oral intubation induced neoplasia in the forestomach after 30 weeks in more than 90% of treated animals. However, no tumors occurred at that site if 1% disulfiram was added to the experimental diet. This inhibition of tumor formation was paralleled by a large inhibition of macromolecular binding of [3H]BP and [14C]BP to RNA and protein in the forestomach. The inhibitory effect of specific binding was strongest in the RNA fraction isolated at 8,000 X g for 20 minutes (6 times that of the control) and weakest in the DNA fraction (no significant difference). The highest specific binding was measured in the RNA fraction isolated at 32,000 X g for 120 minutes and the lowest binding in the DNA fraction. The relative distribution of the BP binding was such that greater than 90% of the BP was bound to protein and less than 1% was bound to DNA. Of the total inhibition of BP binding to all the macromolecular species studied, that to protein constituted the largest component (95%). In contrast to the forestomach, no inhibitory effect of BP binding to DNA, RNA, or protein by disulfiram was found in the liver, which remained free of cancer under the experimental conditions employed.

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The injection of ethanol (70 mmol/kg body weight) into male Wistar rats fed ad libitum caused an increase within 15 min in the liver inorganic pyrophosphate (PPi) content from 0.012 +/- 0.001 mumol/g (wet weight) to 0.029 +/- 0.001 mumol/g. The injection of acetate (20 mmol/kg body weight) increased the liver PPi to 0.157 +/- 0.075 mumol/g in 15 min. The alcohol dehydrogenase inhibitor 4-methylpyrazole blocked the accumulation of acetate and the increase in PPi was prevented. Disulfiram, an inhibitor of aldehyde dehydrogenase, did not prevent changes in redox state, but the accumulation of acetate in the liver was decreased and the increase in liver PPi content was diminished (0.019 +/- 0.003 mumol/g). These data suggest that the increase in PPi observed after injection of ethanol may be due to the activation of the acetate produced during ethanol and acetaldehyde oxidation.

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An NAD(P)-dependent 3 alpha-hydroxysteroid dehydrogenase (EC was purified to homogeneity from rat liver cytosol, where it is responsible for most if not all of the capacity for the oxidation of androsterone, 1-acenaphthenol and benzenedihydrodiol (trans-1,2-dihydroxycyclohexa-3,5-diene). The dehydrogenase has many properties (substrate specificity, pI, Mr, amino acid composition) in common with the dihydrodiol dehydrogenase (EC purified from the same source [Vogel, Bentley, Platt & Oesch (1980) J. Biol. Chem. 255, 9621-9625]. Since 3 alpha-hydroxysteroids are by far the most efficient substrates, the enzyme is more appropriately designated a 3 alpha-hydroxysteroid dehydrogenase. It also promotes the NAD(P)H-dependent reductions of quinones (e.g. 9,10-phenanthrenequinone, 1,4-benzoquinone), aromatic aldehydes (4-nitrobenzaldehyde) and aromatic ketones (4-nitroacetophenone). The dehydrogenase is not inhibited by dicoumarol, disulfiram, hexobarbital or pyrazole. The mechanism of the powerful inhibition of this enzyme by both non-steroidal and steroidal anti-inflammatory drugs [Penning & Talalay (1983) Proc. Natl. Acad. Sci. U.S.A. 80, 4504-4508] was examined with several substrates. Most non-steroidal anti-inflammatory drugs are competitive inhibitors (e.g. Ki for indomethacin, 0.20 microM for 9,10-phenanthrenequinone reduction at pH 6.0, and 0.835 microM for androsterone oxidation at pH 7.0), except for salicylates, which act non-competitively (e.g. Ki for aspirin, 650 microM for androsterone oxidation). The inhibitory potency of these agents falls sharply as the pH is increased from 6 to 9. Most anti-inflammatory steroids are likewise competitive inhibitors, except for the most potent (betamethasone and dexamethasone), which act non-competitively. The enzyme is inhibited competitively by arachidonic acid and various prostaglandins.

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From eight New England Veterans Integrated Service Network centers, 754 patients were dispensed disulfiram, and 971 Asacol Generic Medication were dispensed naltrexone, encompassing 873 and 1075 treatment episodes, respectively. Treatment episode durations were virtually identical for both drugs: more than 35% of episodes were 1 month or shorter, more than 50% were 2 months or shorter, and 75% were 5 months or shorter. Concurrently prescribed neuroleptic or statin medications predicted longer disulfiram and naltrexone treatment episodes. However, for patients newly prescribed common neuroleptic, antidepressant, or statin agents, the risks for discontinuing disulfiram or naltrexone were 1.4 to 2.3 times greater than for discontinuing these other agents.

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Two tests of stimulation of growth hormone secretion were performed in 3 groups of normal Zetia Cost children. In the first test L-Dopa was used on its own; in the second, L-Dopa was combined with Benserazide (group A), with Disulfirame (group B), or with Propranolol (group C). In group A the mean peak value after L-Dopa was 9.1 +/- 1.6 ng/ml; with the combination of L-Dopa and Benserazide it was 12.4 +/- 2.4 ng/ml. The difference between the means is not significant. In group B the mean peak value after L-Dopa was 8.9 +/- 3.6 ng/ml; with the combination of L-Dopa and Disulfirame it was 14.5 +/- 4.4 ng/ml. The difference is not significant. In group C the mean peak value after L-Dopa was 9.8 +/- 2.6 ng/ml; with the combination of L-Dopa and Propranolol, it was 10.1 +/- 1.9 ng/ml. Again the difference is not significant. These findings do not provide evidence in favour of the effect of L-Dopa on the secretion of growth hormone being facilitated by an inhibitor of L-Dopa decarboxylase (Benserazide) or of Dopamine beta hydroxylase (Disulfirame), or by a beta blocking agent (Propranolol). The mechanisms of action of L-Dopa and of the various combinations studied are discussed.

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No in-vitro studies, animal Singulair Online models, reports of adverse effects or clinical studies provide any convincing evidence of a disulfiram-like interaction between ethanol and metronidazole.

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Neuroimaging, particularly MR imaging, plays a major role Imitrex Injections Cost for the diagnosis of many acute toxic encephalopathies. Toxic disorders are related to drugs (immunosuppressive agents, chemotherapeutic agents, anti-epileptic drugs, heroin...), to metals (lead, manganese, mercury...), and to industrial and environmental chemicals (solvent, carbon monoxide...). MR imaging with diffusion and perfusion imaging provides information regarding brain lesions induced by the toxic agents (vasogenic edema, cytotoxic edema, infarction, hemorrhage, demyelination...).

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The transfer of radioactivity from N-nitroso-[14C]dimethylamine to trichloroacetic acid precipitable macromolecules in the microsomal fraction of rat Propecia Buy Online liver was investigated. This transfer was found to depend on N-nitrosodimethylamine being metabolized. Cytosolic fraction and cytosol enriched with reduced glutathione inhibited the binding of radioactivity to acid insoluble proteins. Depletion of glutathione in rat liver with diethylmaleate prior to i.v. administration of 10 mg N-nitroso-[14C]dimethylamine/kg led to an increase in O6-methylguanine and N-7-methylguanine in DNA. If rats were fed disulfiram for 6 days (2 g/kg feed), glutathione and glutathione S-transferase were enhanced, and the degree of methylation of guanine by N-nitrosodimethylamine was greatly reduced, as was the metabolism of N-nitrosodimethylamine in the intact animal. Fasting rats for 24 h did not change the N-nitrosodimethylamine-demethylase activity in vitro but greatly enhanced the methylation of guanine in vivo, while the glutathione content and glutathione S-transferase activity were not changed compared to fed animals.

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Despite the success of combination antiretroviral therapy (cART), HIV persists in Famvir Online Prescription long lived latently infected cells in the blood and tissue, and treatment is required lifelong. Recent clinical studies have trialed latency-reversing agents (LRA) as a method to eliminate latently infected cells; however, the effects of LRA on the central nervous system (CNS), a well-known site of virus persistence on cART, are unknown. In this study, we evaluated the toxicity and potency of a panel of commonly used and well-known LRA (panobinostat, romidepsin, vorinostat, chaetocin, disulfiram, hexamethylene bisacetamide [HMBA], and JQ-1) in primary fetal astrocytes (PFA) as well as monocyte-derived macrophages as a cellular model for brain perivascular macrophages. We show that most LRA are non-toxic in these cells at therapeutic concentrations. Additionally, romidepsin, JQ-1, and panobinostat were the most potent at inducing viral transcription, with greater magnitude observed in PFA. In contrast, vorinostat, chaetocin, disulfiram, and HMBA all demonstrated little or no induction of viral transcription. Together, these data suggest that some LRA could potentially activate transcription in latently infected cells in the CNS. We recommend that future trials of LRA also examine the effects of these agents on the CNS via examination of cerebrospinal fluid.

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The effect of feeding disulfiram (DSF) to rats on the metabolism of N-butyl-N-(4-hydroxybutyl)nitrosamine (BHBN) was examined in order to study the mechanism by which DSF inhibits bladder cancer induction by BHBN. After 2 weeks of feeding 0.5% DSF in the diet, animals were given [14C]BHBN (25 mg/kg) and the urine and expired CO2 were collected for 8 h. Radioactivity in expired air was very low, but DSF caused a significant reduction in expired 14CO2 (control 1.0% of dose; DSF 0.6%), presumably by inhibition of alpha-hydroxylation pathways. There was no difference in the excretion of total urinary radioactivity (control 84%; DSF 85%). Urine was analyzed by h.p.l.c. for BHBN, N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), N-butyl-N-2-hydroxy-3-carboxypropyl)nitrosamine (BHCPN) and N-butyl-N-carboxymethylnitrosamine (BCMN). DSF did not alter the urinary excretion of BCPN (control 64% of dose; DSF 61%), whereas BHCPN excretion was increased (control 11% of dose; DSF 22%) and urinary levels of BCMN were decreased (control 10% of dose; DSF 4%). The metabolism of BHBN was Levitra Cost also studied in isolated hepatocytes from control and DSF-fed rats. Hepatocytes were incubated in Liebovitz's L-15 medium containing 0.5 mM [14C]BHBN and aliquots of the medium were removed for h.p.l.c. analysis at 0.5, 1, 2 and 4 h. Metabolic rates are expressed as mumol/h/5 million cells. There was no difference in the overall rate of metabolism of BHBN in control and DSF-fed rats. BHBN was very rapidly oxidized to BCPN and the rate was not affected by DSF treatment (control 1.82; DSF 1.76). The rate of accumulation of BHCPN was increased 3.5-fold in the DSF-fed rats (control 0.06; DSF 0.21) and BCMN could not be detected. Taken together, these data show that (i) DSF may inhibit the low extent of alpha-hydroxylation of BHBN or BCPN; (ii) DSF does not inhibit the rapid oxidation of BHBN to BCPN and (iii) DSF appears to inhibit the metabolism of BHCPN.

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Although studies repeatedly demonstrate that alcoholics who consistently take disulfiram experience more favorable drinking outcomes, serious problems with compliance among the majority of alcoholic patients have reduced the effectiveness of disulfiram as a therapeutic adjunct. In general, alcoholism counseling with disulfiram simply prescribed seems no more effective than counseling without disulfiram (Fuller et al. 1986). Problems with compliance as well as problems with acceptance by patients and likely by clinical staff reduce the utility of disulfiram in the treatment of alcoholism. Implants, incentives, and various forms of observed or supervised disulfiram have been studied as possible solutions to the problems with compliance. Disulfiram implants appear largely ineffective due to failure to release adequate levels of disulfiram and risks of surgical complications and rejection. Newer techniques (see Allen and Litten 1992) may ultimately lead to a more effective implant. Incentives with personally relevant and obvious reinforcement value such as money, avoidance of incarceration, remaining employed, and continuation of methadone for opiate addicts, have been used effectively. Enhancement strategies with less tangible incentives also show promise. Among these are feedback on results of biochemical measures of disulfiram compliance and continuation in a familiar treatment program. Although each of the studies of incentives suffers from specific methodological limitations, the findings uniformly demonstrate better disulfiram compliance, less drinking, and better clinical outcomes for those who received a meaningful incentive for taking disulfiram. External monitoring of the patient taking disulfiram to assure compliance is typically used in studies evaluating incentives for taking the medication. Observed or supervised disulfiram in its own right and without tangible incentives also has received increasing attention as a method for enhancing compliance. Incorporation of such a strategy would seem to have potential for wide applicability in alcoholism treatment programs. Three forms of supervised disulfiram have been studied: (1) Colorado Botox Cheap a written disulfiram contract, such as in BMT, with instructions about the benefits of the disulfiram contract and methods to establish disulfiram use as a daily habit and specifying that the alcoholic will take disulfiram daily while the spouse observes, that the couple will mutually thank each other, and that they will refrain from arguments or discussions about the alcoholic's drinking; (2) the disulfiram contract used in CRA, which is identical in form to the BMT contract except that talk about drinking is not prohibited; and (3) supervised disulfiram without a written contract, special instructions, or explicit verbal thanking. Studies of these three forms of observed disulfiram have been among the better controlled studies. Each approach has produced very promising results. A disulfiram contract with BMT produced less short-term drinking than disulfiram accompanied either by couples or individual counseling. Unfortunately, the superior BMT drinking results eroded because many couples discontinued their disulfiram contract after treatment ended (O'Farrell et al. 1985, 1992). Adding couples RP sessions after BMT led to better fulfillment of the disulfiram contract and better drinking and marital outcomes than BMT alone. These better RP outcomes persisted for 18 to 24 months after BMT for the entire sample and throughout the entire 30-month followup after BMT for those with more severe drinking and marital problems (O'Farrell et al. 1993). Thus, disulfiram contracts used with BMT are associated with less drinking and greater disulfiram compliance, while the specific contribution of disulfiram contracts to BMT remains to be investigated.(ABSTRACT TRUNCATED AT 400 WORDS)

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The analysis of the global thiol-disulfide redox status in tissues and cells is a challenging task since thiols and disulfides can undergo artificial oxido-reductions during sample manipulation. Because of this, the measured values, in particular for disulfides, can have a significant bias. Whereas this methodological problem has already been addressed in samples of red blood cells and solid tissues, a reliable method to measure thiols and disulfides in cell cultures has not been previously reported. Here, we demonstrate that the major artifact occurring during thiol and disulfide analysis in cultured cells is represented by glutathione disulfide (GSSG) and S-glutathionylated proteins (PSSG) overestimation, due to artificial oxidation of glutathione (GSH) during sample manipulation, and that this methodological problem can be solved by the addition of N-ethylmaleimide (NEM) immediately after culture medium removal. Basal levels of GSSG and PSSG in different lines of cultured cells were 3-5 and 10-20 folds higher, respectively, when the cells were processed without NEM. NEM pre-treatment also prevented the artificial reduction of disulfides that occurs during the pre-analytical phase when cells are exposed to an oxidant stimulus Cytoxan Iv Cost . In fact, in the absence of NEM, after medium removal, GSH, GSSG and PSSG levels restored their initial values within 15-30 min, due to the activity of reductases and the lack of the oxidant. The newly developed protocol was used to measure the thiol-disulfide redox status in 16 different line cells routinely used for biomedical research both under basal conditions and after treatment with disulfiram, a thiol-specific oxidant (0-200 μM concentration range). Our data indicate that, in most cell lines, treatment with disulfiram affected the levels of GSH and GSSG only at the highest concentration. On the other hand, PSSG levels increased significantly also at the lower concentrations of the drug, and the rise was remarkable (from 100 to 1000 folds at 200 μM concentration) and dose-dependent for almost all the cell lines. These data support the suitability of the analysis of PSSG in cultured cells as a biomarker of oxidative stress.