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Antabuse (Disulfiram)

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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:

Similar Products:
Camprall, Naltrexone, Vivitrol


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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This article reviews the literature on alcohol and medication interactions, with a focus on older adults.

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Mushrooms are ubiquitous in nature. They are an important source of nutrition, however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, whereas foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I reviewed the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and presented an overview of the cyclopeptide-containing mushroom class. Part II is focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.

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Retinoic acid is synthesized from retinaldehyde by several different dehydrogenases, which are arranged in conserved spatial and developmentally regulated patterns. Here we show for the mouse that a class-1 aldehyde dehydrogenase, characterized by oxidation and disulfiram sensitivity, is found in the brain at high levels only in the basal forebrain. It is present in axons and terminals of a subpopulation of dopaminergic neurons of the mesostriatal and mesolimbic system, forming a retinoic acid-generating projection from the ventral tegmentum to the corpus striatum and the shell of the nucleus accumbens. In the striatum the projection is heaviest to dorsal and rostral regions, declining gradually toward ventral. The enzyme is expressed early in development, shortly after appearance of tyrosine hydroxylase. Other dopaminergic neurons in the brain, as well as the chromaffin cells of the adrenal medulla, do not contain this dehydrogenase. The presence of this enzyme may be a factor in the long-term success of transplants of dopaminergic cells to the corpus striatum in Parkinson disease, and it may play a role in parkinsonism and catatonia due to disulfiram (Antabuse) neurotoxicity.

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The study examined the feasibility of screening for hepatotoxicity by an in vitro gene expression analysis using rat primary hepatocytes and Affymetrix Rat Toxicology U34 arrays. Hepatocytes were exposed for 6 or 24 h to eight drugs, with different mechanisms of hepatotoxicity, at one third of the cytotoxic concentration TC50, i.e. acetaminophen, cyclophosphamide, clofibrate, chlorpromazine, lithocholic acid, cisplatin, diclofenac and disulfiram. The types of transcriptional changes observed in this study were generally consistent with previously reported in vivo data, although there were some differences. In hierarchical cluster analysis, drugs formed clusters depending on their mode of toxicity against cells. The number of transcripts affected by the cholestatic hepatotoxicants (lithocholic acid and chlorpromazine) or the drugs that rarely cause of hepatotoxicity (cisplatin, diclofenac and disulfiram) were limited compared with the other drugs (acetaminophen, clobifibrate and cyclophosphamide), where they did not induce transcriptional changes apparently related to toxicity. It is concluded that in vitro gene expression analysis of hepatocytes using microarray is a useful tool for evaluating the toxicological profile of drugs and in screening for the direct toxicity of drugs against hepatocytes.

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In experimental animals, diethyldithiocarbamate as well as carbon disulfide exert antihepatotoxic effects in different models of chemically-induced liver injury like carbon tetrachloride, chloroform, bromobenzene, dimethyl nitrosamine, furosemide, D-galactosamine, paracetamol, thioacetamide and trichloroethylene. On the other hand, both dithiocarb and CS2 are strong inhibitors of the microsomal mixed-function oxidase system which is involved in the bioactivation of these hepatotoxic agents. It is concluded that CS2 and CS2-producing agents as dithiocarb and disulfiram may inhibit metabolism of other xenobiotics and, thereby, not only protect against various hepatotoxic compounds that require bioactivation but also affect efficacy and duration of action of many drugs.

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The CT or TT MTHFR genotype group (N = 32) dropped from 73 to 52% cocaine-positive urines on disulfiram (p = 0.0001), while the placebo group showed no treatment effect. The CC MTHFR genotype group (N = 24) showed a smaller, but still significant, reduction in cocaine-positive urines on disulfiram compared to placebo; 81-69% (p = 0.007).

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Baseline subject characteristics, retention and drug use did not differ across groups. Outcome analyses were performed on those who participated beyond week 2. Opioid-positive urine samples and self-reported opioid use did not differ by treatment group. The prevalence of alcohol use was low prior to and during the trial and did not differ by treatment group. Cocaine-positive urines increased over time in the 62.5 and 125 mg disulfiram groups and decreased over time in the 250 mg disulfiram and placebo groups (p < 0.0001). Self-reported cocaine use increased in the 125 mg disulfiram group relative to the other three treatment groups (p = 0.04).

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Postoperative complications requiring treatment within the first month after surgery. Perioperative immunosuppression measured by delayed type hypersensitivity; myocardial ischaemia and arrhythmias measured by Holter tape recording; episodes of hypoxaemia measured by pulse oximetry. Response to stress during the operation were assessed by heart rate, blood pressure, serum concentration of cortisol, and plasma concentrations of glucose, interleukin 6, and catecholamines.

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The effects of cephem antibiotics and their related compounds on aldehyde dehydrogenase obtained from rat liver mitochondria were studied. A pH of 8.8 and reaction temperature 24 degrees were the conditions for measurement of enzyme activity. The apparent Michaelis constant Km values for NAD, acetaldehyde and propionaldehyde were 3.8 X 10(-5) M, 4.0 X 10(-5) M and 2.5 X 10(-5) M, respectively. Cefamandole, cefoperazone and cefmetazole, having a 1-methyl-5-thiotetrazol group at position 3 of the cephem ring, caused a relatively potent inhibition of aldehyde dehydrogenase. Cefmetazole and cefoperazone also showed a significant inhibition on highly purified yeast aldehyde dehydrogenase; the extent of inhibition on yeast enzyme was almost the same as that on rat mitochondrial aldehyde dehydrogenase. The decrease in enzyme activity effected by 1-methyl-1H-tetrazol-5-thiol (MTT) was greater than those of 1H-tetrazol (TZ), 1H-tetrazol-5-thiol and 1-(2-dimethylaminoethyl)-1H-tetrazol-5-thiol, but was, of course, less than that of disulfiram. Cefamandole, cefmetazole and MTT showed competitive inhibition with NAD, while TZ was uncompetitive inhibitor with respect to both NAD and acetaldehyde. Enzyme inhibition caused by disulfiram, cefmetazole and MTT increased time-dependently and the addition of 2-mercaptoethanol into the medium effectively and completely restored enzyme inhibition. These results suggest that thiol group at position 5 of 1H-tetrazol ring is responsible for the type of inhibition with NAD, and methyl group at position 1 of 1H-tetrazol ring is important to exhibit a potent inhibition on aldehyde dehydrogenase.

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Individuals with alcohol use disorders (AUDs) have deficits in cognitive control, but how they change with treatment is unclear. Seven patients with AUD and anxiety from an open-label trial of disulfiram plus lorazepam performed a multisensory Stroop task during fMRI (both pre and post initiation of treatment), and were compared to nine healthy controls (HCs) (n = 16; Albuquerque, NM; years 2009-2012). Evoked BOLD signal and resting state functional connectivity were compared (HC vs. AUD; Scan 1 vs. Scan 2). AUD demonstrated hyperactivity and altered connectivity in the cognitive control network compared to HC, but treatment did not normalize function.

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The levels of high molecular weight (HMW) kininogen and pre-kallikrein in rat plasma were markedly reduced after single injection of bromelain (10 mg/kg, i.v.) and gradually recovered over a 72 hour period. The level of low molecular weight (LMW) kininogen, however, was not changed during this period. Rat pleurisy was induced by intrapleural injection of lambda-carrageenin. The levels of HMW kininogen and prekallikrein, but not of LMW kininogen, in the exudate were markedly decreased, when compared with those in plasma of the same animals. After pretreatment with disulfiram, oral administration of ethanol (2 g/kg) or intravenous injection of acetaldehyde (10 mg/kg) to rats caused significant decrease in the plasma level of LMW kininogen with no significant effect on the plasma HMW kininogen and prekallikrein levels. These results suggest that HMW and LMW kininogens may be consumed separately in vivo and play different roles.

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A low frequency stimulation of the head of the caudate nucleus in freely moving cats leads to an arrest of reactions with an increased muscular tone and tremor. This reaction may serve as an experimental model of one of the expressions of parkinsonism, inasmuch as its accomplishment depends upon the central dopaminergic mechanisms (confirmed on experiments with disulfiram and alpha-methyltyrosine). The similarity is also supplemented by the fact that the arrested reaction is weakened by antiparkinson drugs (d, 1-amphetamine, DOPA, artane) and is increased by neuroeptical preparation (aminazine, haloperidol, reserpine).

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In a single-blinded, randomized placebo-controlled study, we recruited 109 patients diagnosed with alcohol dependence under ICD-10 criteria. The patients were randomly allocated to 4 treatment groups, depending on whether they took disulfiram (200 mg daily) or a placebo or whether they received adjunctive therapy consisting of mailed letters which delineated and emphasized the harmful effect of alcohol and the management of alcohol craving. The proportion of abstinence among the 4 groups at 26 weeks after discharge was the primary outcome measure. The proportion of abstinence was compared with the severity of alcohol dependence and craving. Furthermore, we examined the proportion of abstinence in patients with inactive aldehyde dehydrogenase-2 (ALDH2).

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The disposition of chlordiazepoxide, diazepam, oxazepam and lorazepam was studied before and after disulfiram administration to normal subjects and alcoholic patients. Similar studies to determine the effect of ethanol administration on diazepam and oxazepam disposition were also performed. After disulfiram, decreases in the plasma clearance of chlordiazepoxide (54%, p < 0.05; diazepam, 41% p < 0.05) and their active metabolites were observed. Oxazepam and lorazepam have no important active metabolites and the effect of disulfiram on their net disposition was minimal. In normal subjects ethanol (> 800 mg/l maintained for 8 h) increased the AUC free diazepam (26.6 +/- 17.3% mean +/- SD, p < 0.05) and decreased the AUC for N-desmethyldiazepam (50.5 +/- 11.7%, p < 0.05) indicating inhibition of diazepam N-desmethylation. In contrast, there was no significant change in the disposition of oxazepam in four healthy subjects after a single oral dose of ethanol. Thus, disulfiram and ethanol appear not to inhibit the metabolic disposition of oxazepam or lorazepam, benzodiazepine derivatives principally biotransformed by glucuronidation. On pharmacokinetic grounds oxazepam and lorazepam may be the drugs of choice if benzodiazepine therapy is required in chronic alcoholics.

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The interaction between the alcohol assumption and industrial chemicals may be toxicokinetic or toxicodynamic. Alcohol can interfere in the processes of biotransformation of xenobiotics and modify the doses and the effect indicators used for the biological monitoring, causing wrong interpretations of the results. The metabolism of ethanol can be altered by the exposures to toxic industrial materials, creating some clinical pictures of alcohol intolerance, like an "antabuse syndrome" or an "degreaser flush syndrome". Professional exposure to carbon sulfide or to dimethylformamides, trichloroethylene as well as to nitroglycerin and nitroglycole ethylenic can produce similar syndromes. Interactions are reported between alcohol and solvents: on toxicokinetic bases for methanol, isopropanol, glycol ether, trichloroethylene, methyl ethyl ketone and toluene; and on toxicodynamic bases for CNS. Also between alcohol and metals there can occur toxicokinetic interactions, like in the case of lead and mercury. Alcohol can also interfere with the biological monitoring of solvents, producing an over-estimation of the exposure.

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In this largest cost study to date of alcohol pharmacotherapy, patients who received medication had lower healthcare utilization and total costs than patients who did not. XR-NTX showed an advantage over oral medications in treatment persistence and healthcare utilization, at comparable or lower total cost.

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An ex vivo model was established which allows the testing of drugs on lens epithelial cell ablation. Drug treatment reduced the number of viable cells on the specimens drastically, ranging between 0.44 ± 0.53% (6.0 ± 7.3 cells/mm²) for disulfiram, 0.27 ± 0.50% (3.7 ± 6.9 cells/mm²) for methotrexate and 0.07 ± 0.19% (0.1 ± 0.27 cells/mm²) for actinomycin D. Rabbit eyes treated with a mixture of methotrexate/actinomycin D showed no posterior capsule opacification at 4 months and a low opacification 6 months postoperatively. Without drug treatment low opacification starts 6 weeks postoperatively.

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Alcohol dependence is a widespread, chronic disorder with enormous health consequences. Psychological and behavioral therapies have been the mainstay of treatment and are demonstrated to be effective, but they do not lead to reduced drinking or abstinence in all patients. Advances in neurobiology have led to the identification of drug targets and the development of novel drugs to treat alcohol dependence, and many patients will benefit from the addition of pharmacotherapy to their treatment regimen. Pharmacologic treatment options for use in conjunction with psychotherapy include the aversion-based therapy disulfiram, the opioid receptor antagonist naltrexone, and acamprosate, which is thought to act by normalizing the glutamate and gamma-aminobutyric acid neurotransmitter systems. The effectiveness of pharmacotherapies depends on adherence, which is often poor in alcohol-dependent patients. Recently, a monthly, extended-release formulation of naltrexone has been approved for alcohol dependence, which promises to minimize nonadherence, a problematic factor in the management of alcohol dependence.

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Hepatitis serologies and baseline transaminase levels were obtained for 57 male alcoholics starting treatment with disulfiram. Sequential liver function test results were obtained for up to 12 weeks while subjects took disulfiram.

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Acetaldehyde is the first and principal metabolite of ethanol administered systemically. To its rise in blood, after administration of disulfiram, is ascribed the aversive reaction that should discourage alcoholics from drinking. In the present study, we sought to determine the effect of acetaldehyde on the electrophysiological properties of dopamine (DA)-containing neurons in the ventro tegmental area (VTA) of rats in vivo. Intravenous (i.v.) administration of acetaldehyde (5-40 mg/kg) readily and dose-dependently increased the firing rate, spikes/burst, and burst firing of VTA neurons. Ethanol (250-1000 mg/kg/i.v.) administration produced similar increments in electrophysiological parameters. In addition, a second group of rats was pretreated with the alcohol-dehydrogenase inhibitor 4-methyl-pyrazole (90 mg/kg) intraperitoneally (i.p.), and ethanol and acetaldehyde were administered i.v. at the same doses, 48 h later. In this group, ethanol effects were drastically reduced and the firing rate, spikes/burst, and burst firing were not significantly altered. In contrast, acetaldehyde fully retained its capacity to stimulate electrophysiological indices. The results indicate that acetaldehyde produces electrophysiological actions on VTA neurons in vivo, similar to those produced by ethanol, and significantly participate in ethanol-induced increment in DA neuronal activity. These results also suggest that acetaldehyde, by increasing DA neuronal activity in the VTA, may significantly contribute to the centrally mediated positive motivational properties of ethanol, which would oppose the well-known peripherally originating aversive properties.

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The oral administration with DSF suppressed, in a dose-dependent manner, the number of inflammatory cells, the protein concentration, and the levels of TNF-α, NO, and PGE2 in the aqueous humor and improved the histiologic status of the ocular tissue. The expression of activated NF-κB-positive cells in the ICB was significantly inhibited by oral administrated with DSF 3 hr after the LPS injection. The LPS-induced increased expressions of iNOS and COX-2 proteins in the ICB were also inhibited by oral DSF 24 hr after LPS injection.

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We have reported previously that diethyldithio-carbamate (DDC) and pyrrolidine dithiocarbamate (PDTC) induce apoptosis in rat thymocytes. Apoptosis was shown to be dependent upon the transport of external Cu ions into the cells and was accompanied by the oxidation of intracellular glutathione, indicating the inducement of pro-oxidative conditions (C. S. I. Nobel, M. Kimland, B. Lind, S. Orrenius, and A. F. G. Slater, J. Biol. Chem. 270, 26202-26208, 1995). In the present investigation we have examined the chemical reactions underlying these effects. Evidence is presented to suggest that dithiocarbamates undergo oxidation by CuII ions, resulting in formation of the corresponding thiuram disulfides, which are then reduced by glutathione, thereby generating the parent dithiocarbamate and oxidized glutathione (glutathione disulfide). Although DDC and PDTC were found to partially stabilize CuI ions, limited redox cycling of the metal ion was evident. Redox cycling did not, however, result in the release of reactive oxygen species, which are believed to be scavenged in situ by the dithiocarbamate. DDC and PDTC were, in fact, shown to prevent copper-dependent hydroxyl radical formation and DNA fragmentation in model reaction systems. The thiuram disulfide disulfiram (DSF) was found to induce glutathione oxidation, DNA fragmentation, and cell killing more potently than its parent dithiocarbamate, DDC. Of particular importance was the finding that, compared with DDC, the actions of DSF were less prone to inhibition by the removal of external copper ions with a chelating agent. This observation is consistent with our proposed mechanism of dithiocarbamate toxicity, which involves their copper-catalyzed conversion to cytotoxic thiuram disulfides.

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The use of a number of antibiotics which contain an N-methyl-thiotetrazole (NMTT) side chain has been reported to be associated with an increased incidence of hypoprothrombinemia. The suggested role of NMTT as an inhibitor of the liver microsomal vitamin K-dependent carboxylase has been investigated. In standard incubations, NMTT had no effect on carboxylation when vitamin KH2 was a substrate but was a weak inhibitor when [vitamin K + NADH] was a substrate. Microsomal vitamin K reductases, however, were not inhibited by NMTT. Preincubation of the incubation mixture with NADH and NMTT resulted in inhibition of carboxylase activity when either vitamin KH2 or [vitamin K + NADH] was the substrate. A fraction of the microsomal membrane which was not readily solubilized by dilute detergent protected the enzyme from this inhibition. The data suggest that NMTT is metabolized to an active inhibitor or is able to covalently inactivate the enzyme in the presence of NMTT. The vitamin K responsiveness of the clinically observed hypoprothrombinemia suggests that it is not related to this in vitro inhibition of the vitamin K-dependent carboxylase.

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Alcohol abusers have suppressed cellular immune function. The aim of the study was to investigate the time of sobriety required to normalize immune function. Delayed hypersensitivity was investigated during disulfiram controlled abstinence in ten heavy alcoholics and in seven moderate drinkers without liver diseases. For comparison a control group of eight previous drinkers was tested. The skin test responses were modest initially with a median area of response of 12 mm2 (range 0-31) in the heavy alcoholics and 3 mm2 (0-15) in the moderate drinkers. It improved significantly in both groups after two weeks of sobriety. The responses stabilized after 8 weeks at 74 mm2 (54-102) in the heavy alcoholics and after 9 weeks at 63 mm2 (42-76) in the moderate drinking group. The control group had skin test responses of 70 mm2 (46-87), not different from the responses of the alcohol groups after two months of abstinence. The results suggest that while 2 weeks of abstinence from alcohol will improve the depressed cellular immunity, 2 months of sobriety is necessary to normalize it.

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The influence of a 28-week treatment with disulfiram (DSF), D-penicillamine (PA), and nitrosodiethylamine (NDEA), as well as with a combination of DSF or PA with NDEA on the concentrations of eight essential trace elements in the whole liver tissue of rats was measured by means of neutron activation analysis. While NDEA treatment lowered the Zn content of the liver, DSF alone or in combination with NDEA enhanced the Zn and Se concentration by 50%-80%. Co, Cu, and Cd levels were increased by factors of 10, 60, and 110, respectively. The Mo concentration was decreased by 50% after DSF administration. PA reduced Cu, Co, and Zn in the liver. PA/NDEA treatment also lowered Cu, Co, and Zn content, but there was no strengthening effect of PA on the decrease in Zn observed with NDEA. The change of trace element concentrations, especially of Cu, is discussed with regard to the observed tumor induction in the liver, which tended to be increased by a combined NDEA/PA administration compared with NDEA treatment alone, whereas a protective action of DSF against NDEA induced liver tumors could not be established.

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The use of combination chemotherapy is the accepted standard for most human malignancies but little attention has been paid to drug interactions. A combination of drugs may be synergistic, additive, or antagonistic in cytotoxic activity. This study evaluated combinations of agents with docetaxel, one of the most active agents in human breast cancer, using a median effects model to look at synergy or antagonism in vitro as a potential predictor of clinical outcome. Three human breast cancer cell lines, MCF7/wt, MCF7/adr (multiply drug resistant), and BT474 were grown to confluence, plated into 96 well dishes, and incubated with combinations of drugs for 72h. Cytotoxic effect was measured by the MTT assay. Median effect analysis was used to calculate the combination index (CI) with values less than 1 indicating synergism, 1 additive effects, and greater than 1 antagonism. Potentially useful combinations for clinical study which were identified included docetaxel with vinorelbine, docetaxel with dexrazoxane, docetaxel with cis-retinoic acid, docetaxel with disulfiram and either doxorubicin or epirubicin, and docetaxel with dexrazoxane and epirubicin.

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The identification of genes inducing resistance to anticancer chemotherapeutic agents and their introduction into hematopoietic cells represents a promising approach to overcome bone marrow toxicity, the limiting factor for most high-dose chemotherapy regimens. Because resistance to cyclophosphamide has been correlated with increased levels of expression of the aldehyde-dehydrogenase (ALDH1) gene in tumor cell lines in vitro, we tested whether ALDH1 overexpression could directly induce cyclophosphamide resistance. We have cloned a full-length human ALDH1 cDNA and used retroviral vectors to transduce it into human (U937) and murine (L1210) hematopoietic cell lines that were then tested for resistance to maphosphamide, an active analogue of cyclophosphamide. Overexpression of the ALDH1 gene resulted in a significant increases in cyclophosphamide resistance in transduced L1210 and U937 cells (50% inhibition concentration [IC50], approximately 13 mumol/L). The resistant phenotype was specifically caused by ALDH1 overexpression as shown by its reversion by disulfiram, a specific ALDH1 inhibitor. ALDH1 transduction into peripheral blood human hematopoietic progenitor cells also led to significant increases (4- to 10-fold; IC50, approximately 3 to 4 mumol/L) in cyclophosphamide resistance in an in vitro colony-forming assay. These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo.

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antabuse drug cost 2015-03-07

To review medication adherence rates with various pharmacotherapies and the role of pharmacists in improving buy antabuse medication adherence in patients with alcohol dependence.

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In an attempt to dissociate the chemotherapeutic from the carcinogenic properties of the antischistosomal and antitrypanosomal nitrovinylfuran trans-5-amino-3-[2-(5-nitro-2-furyl)vinyl]1,2,4-oxadiazole [(SQ18506) CAS: 28754-68-9; (E)-5-amino-3-(2-(5-nitro-2-furyl)vinyl)-1,2,4-oxadiazole], potential inhibitors of carcinogenesis were administered to female outbred CD-1 mice before and during exposure to SQ18506. The compounds tested were ascorbic acid, etretinate, butylated hydroxyanisole (BHA), cysteamine hydrochloride, cysteine hydrochloride, dimercaprol, disulfiram, 1,4-dithiothreitol, reduced glutathione, and spermidine phosphate. The primary types of tumors observed were squamous cell carcinomas of the stomach and thymic and nonthymic lymphomas. BHA reduced the incidence of malignant tumors to control levels, whereas cysteine hydrochloride, spermidine phosphate, and disulfiram reduced the incidence of chemically induced tumors by 42, 34, and 32%, respectively. Although cysteamine hydrochloride and disulfiram had no or only a modest effect on the overall buy antabuse incidence of tumors, the data suggested possible tissue-specific anticarcinogenic properties for these agents. Of the 8 antioxidants tested, only 1 had marked anticarcinogenic properties against SQ18506. These data indicate that antioxidant properties alone cannot account for the anticarcinogenic activity of the compounds tested. Coadministration of the anticarcinogen BHA with SQ18506 also blocked the chemotherapeutic effects of this agent on female CD-1 mice infected with Schistosoma mansoni.

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The Swedish SBU report, published in English in 2003, was used as a database. It includes 641 randomized controlled trials and buy antabuse seven longitudinal prospective studies.

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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 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 buy antabuse 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.

antabuse dosage instructions 2017-12-07

Antabuse taken under supervision is effective and useful in the treatment of selected patients in the very long term. Relapses during treatment buy antabuse are the rule rather than the exception as is also illustrated in five case reports, but Antabuse treatment contributes to longer periods of sobriety. Continued support by nurses is necessary in the treatment of alcohol dependent patients and appointments with a psychiatrist are important for patients with alcohol dependence and psychiatric disorders. The personal perception of the severity of the drinking problem seems to be of decisive importance for compliance with the treatment. A high degree of motivation to stop drinking leads to long-term use of Antabuse, a stronger internal locus of control and a favourable outcome. Measurements of liver enzymes are useful for monitoring the treatment outcome as well as for detecting toxic effects on the liver.

antabuse 500 mg 2017-08-03

Disulfiram is used buy antabuse to treat alcoholism and is known to cause peripheral neuropathy: few reports of biopsied human nerves have revealed axonal degeneration and loss of myelinated fibers. We studied a 22-year-old woman with severe sensorimotor neuropathy following treatment with disulfiram for 6 months. Histologic studies of the sural nerve revealed a neurofilamentous axonopathy with rare enlarged axons distended by neurofilaments. Disulfiram is converted enzymatically to carbon disulfide, which causes neurofilamentous distal axonopathy in animals. Similar changes in human nerve after disulfiram administration suggest that carbon disulfide is the toxic agent.

antabuse buy online 2015-10-17

Changes in the immunospecificity of the nuclear antigens were demonstrated in the colon chromatin of rats buy antabuse treated with 1,2-dimethylhydrazine. Tumor-specific nuclear antigen appeared in the early stages of chemically induced colon carcinogenesis. Sodium barbiturate, in conjunction with the carcinogen, induced a higher level of nuclear antigen activity than that obtained with carcinogen alone. The rise of immunoactivity in carcinogen-treated colon chromatin can be abolished by simultaneous treatment with disulfiram or butylated hydroxytoluene.

antabuse online pharmacy 2015-10-30

Vitamin E deficiency myopathy (white muscle disease) was induced in 14 suckling lambs (2 experiments; 7 lambs/experiment) by addition of cod liver oil to the diet. Disulfiram buy antabuse , an antioxidant, was administered orally once each day to 8 of the 14 lambs at 2 different doses. Serum creatine kinase (CK) activity was measured weekly for 5 weeks. Increased CK activity was evident in some lambs beginning at week 3. By week 4, serum CK was abnormally increased in 5 of the 6 nontreated lambs (ie, disulfiram not given) and in 4 of the 8 treated lambs. The combined disulfiram groups had significantly lower serum CK values during the study (P less than 0.05). Serum alpha-tocopherol, measured on samples from week 5 for lambs of experiment 1, was significantly higher in treated lambs (P less than 0.01). Microscopic examination of the vastus lateralis muscle indicated that the most severe lesions, consistent with nutritional myopathy, were seen in nontreated lambs. Therefore, disulfiram may have an antioxidant effect in lambs with vitamin E deficiency.

antabuse medication 2017-03-02

Disulfiram is used in alcohol rehabilitation because it inhibits aldehyde dehydrogenase and consequently causes the disulfiram-ethanol reaction (vomiting, vertigo, anxiety, cardiovascular effects) after ingestion of alcoholic beverages. However, adverse effects on the central nervous system (for the most part psychotic reactions, acute organic brain syndrome, catatonia) may appear as a direct result of the drug itself. Disulfiram and its metabolite carbon disulfide inhibit dopamine beta-hydroxylase, increasing the levels of dopamine and reducing those of norepinephrine in the central nervous system. We observed direct disulfiram-induced toxicity on the central nervous system in 8 abstinent patients in whom a disulfiram-ethanol reaction had been excluded. Risk is increased when 1) excessive amounts of the drug are ingested; 2) the patient is already suffering from a major psychiatric illness; 3) the patient has anatomical brain lesions. In all cases observed, the toxic effects appeared in the first weeks and were reversed after suspension of the drug (except in one patient who died from severe bronchopulmonary infection). We thus suggest the following protocol: 1) physical examination and interview 3-4 weeks after initiation of treatment; 2) as a general rule, in abstinent patients, the lowest possible maintenance dosage should be administered. This strategy, despite the risk of underdosage, meets the goals inherent in an integrated medical and psychosocial approach to the treatment of alcoholism with which these patients buy antabuse seem better able to comply.

antabuse and alcohol 2015-04-08

Dopamine (30 and 45 mug) administered intracerebroventricular (i.c.v.) to a group of 10 conscious normotensive cats caused dose-related increases in blood pressure and heart rate. In 4 of these animals the initial cardiovascular stimulant effects of i.c.v. dopamine were followed by hypotension and bradycardia. 2 alpha-Methyldopamine (30 and 45 mug i.c.v.) produced qualitatively similar responses to dopamine except that the cardiovascular stimulant effects were smaller and the secondary depressant effects somewhat more prolonged. 3 Both stimulant and depressant effects of i.c.v. dopamine and alpha-methyldopamine were greatly inhibited by autonomic ganglion blockade or by adrenergic neurone blockade. 4 The cardiovascular stimulant effects of both i.c. buy antabuse v. dopamine and i.c.v. alpha-methyldopamine were selectively inhibited by beta-adrenoceptor blocking agents whilst the cardiovascular depressant effects of these substances were abolished by the alpha-adrenoceptor blocker phentolamine or by the dopamine-beta-hydroxylase inhibitor disulfiram. 5 Haloperidol by either i.c.v. or the intravenous route abolished both cardiovascular stimulant and depressant effects of i.c.v. dopamine, whilst pimozide by either route inhibited only the cardiovascular stimulant effects. 6 In 2 cats, injection of dopamine into the cisterna magna produced predominantly depressant effects on the cardiovascular system except with a higher dose which induced biphasic responses.

disulfiram antabuse reviews 2017-12-09

Fulminant hepatitis is a rare but buy antabuse potentially fatal adverse reaction that may occur after the use of disulfiram. A patient without a known history of liver disease was transplanted for fulminant hepatic failure secondary to disulfiram. A high index of suspicion and aggressive therapeutic approaches are essential for the prompt diagnosis and treatment of disulfiram-induced hepatic failure. The clinical presentation, histopathology, treatment, and all cases of disulfiram-induced hepatic failure reported in the English literature are reviewed. The role of orthotopic liver transplantation in a case of disulfiram-induced hepatic failure is discussed.

antabuse 50 mg 2015-04-28

In the first part of the paper is reported on differential buy antabuse -therapeutic experiences in the hospital treatment of 307 alcoholics with disulfiram R, Lithium R and Apomorphine R as monotherapy as well as in combined application. Our investigations show that neither lithium R nor apomorphine R have ascertained advantages to the monotherapy with Disulfiram R. An improvement of the still unsatisfactory number of success is to be achieved in the first place by an optimization of the after-care by means of a close sociotherapeutic and if necessary psychotherapeutic care, possibly in special outpatient departments. In the second part of the paper is reported on first experiences.

antabuse buy 2017-10-30

The objective of this study is to evaluate differential response to disulfiram treatment of cocaine dependence by sex. Sex by treatment interactions from two pooled randomized clinical trials involving 191 cocaine-dependent subjects (36% female) were evaluated. Primary outcomes were days of abstinence and percentage buy antabuse of drug-free urine specimens. Significant sex by treatment interactions were found, where men treated with disulfiram had better outcomes than those who were not. Women had an intermediate outcome regardless of whether they received disulfiram. Sex differences in response to disulfiram treatment have important clinical and theoretical implications. Reasons for this apparent sex-based response are not clear, but possible mechanisms worthy of greater study include differences in alcohol use by sex as well as differences in dopamine-mediated responses to cocaine and disulfiram.

antabuse tablets 2015-08-05

A combination of medical treatment (naltrexone, acamprosate or disulfiram) with the CBT-booklet (patient guide) appears to help reduce patients' symptoms of depression and improve their QL. Treatment is also associated with success at quitting smoking, buy antabuse especially among patients using disulfiram.

antabuse drug 2016-04-18

We present the case of a 30-year-old man with disulfiram-induced hepatitis complicated by fatal liver failure. The disease followed a protracted course with an interval of 25 days between the onset of jaundice and the onset of Singulair Kids Dosage encephalopathy. In this patient, the severity of the liver disease might have been due to reingestion of disulfiram shortly after the onset of jaundice.

antabuse drug interactions 2017-08-12

Alcohol appears to interact with many drugs in many different and complicated ways. The absorption and metabolism of drugs can be altered under the influence of acute or chronic alcohol intake, and it is possible that alcohol itself Famvir With Alcohol or its metabolic products may interfere with the effect of several drugs. These interactions are not only of biological interest but also of clinical importance, and the general practitioner should therefore be aware of them. The therapy of patients with chronic alcoholism is often complicated by such interactions, and it is thus important to know both the habits of the patient with respect to alcohol intake and possible interference with the drugs used.

antabuse online cheap 2017-05-06

An aggregate sample comprised of data from five randomized clinical trials of treatment for cocaine dependence (N = 434) was evaluated for gender differences in clinical outcomes. Secondary analyses compared gender Zithromax 200 Mg differences in outcome by medication condition (disulfiram versus no medication) and across multiple behavioral treatment conditions.

antabuse recommended dose 2015-05-03

An estimate of amounts of thiurams that may be released from rubber gloves into synthetic sweat, has previously been generated. These amounts should be compared to elicitation thresholds of patch tests performed with serial dilutions of thiuram mix using synthetic sweat as vehicle. Because of solubility properties of thiurams in aqueous media, such dilutions cannot directly be prepared. In this study, a stem solution was prepared in ethanol. This solution was then further diluted with synthetic sweat. Thiuram mix 0.5 w/v% was the most concentrated solution in ethanol achievable. The patch test reactions were compared to reactions to serial dilutions using petrolatum as vehicle. The experiment revealed that endpoint dilution with synthetic sweat was not achieved in this study. The threshold for elicitation of positive patch test reactions seemed to be lower for ethanol/sweat as vehicle Lamictal Missed Dose compared to petrolatum: 32% reacted to ethanol/synthetic sweat 0.001 mg/cm2 compared to 14% reacting to thiuram in pet. 0.002 mg/cm2. Based on these results, synthetic sweat may be considered a more relevant medium for threshold finding studies than petrolatum. Because of expected instability of the aqueous solutions, petrolatum is probably a more suitable vehicle for routine testing. The study does not permit final conclusions concerning acceptable thresholds for leachable thiurams in rubber gloves, but it is likely that an acceptable threshold would be substantially less than 0.001 mg/ cm2.

antabuse overdose 2016-10-13

Amidation is a post- Lopid Starting Dose translational modification found at the C-terminus of ~50% of all neuropeptide hormones. Cleavage of the C(α)-N bond of a C-terminal glycine yields the α-amidated peptide in a reaction catalyzed by peptidylglycine α-amidating monooxygenase (PAM). The mass of an α-amidated peptide decreases by 58 Da relative to its precursor. The amino acid sequences of an α-amidated peptide and its precursor differ only by the C-terminal glycine meaning that the peptides exhibit similar RP-HPLC properties and tandem mass spectral (MS/MS) fragmentation patterns. Growth of cultured cells in the presence of a PAM inhibitor ensured the coexistence of α-amidated peptides and their precursors. A strategy was developed for precursor and α-amidated peptide pairing (PAPP): LC-MS/MS data of peptide extracts were scanned for peptide pairs that differed by 58 Da in mass, but had similar RP-HPLC retention times. The resulting peptide pairs were validated by checking for similar fragmentation patterns in their MS/MS data prior to identification by database searching or manual interpretation. This approach significantly reduced the number of spectra requiring interpretation, decreasing the computing time required for database searching and enabling manual interpretation of unidentified spectra. Reported here are the α-amidated peptides identified from AtT-20 cells using the PAPP method.

antabuse online canada 2017-12-30

1. The effects of various sulphydryl-blocking reagents on aniline biotransformation and cytochrome P-450 Nizoral Cream Dosage levels were studied in cultured rat hepatocytes. 2. Exposure of aniline-metabolizing hepatocytes to p-chloro-mercuribenzoate (PCMB) or p-chloromercuribenzenesulphonic acid (PCMBS) resulted in decreased levels of cytochrome P-450, decreased glucuronidation of 4-aminophenol and increased levels of free 4-aminophenol. 3. Incubation of aniline-metabolizing hepatocytes with disulfiram resulted in decreased formation of 4-aminophenol, but this was not associated with impaired glucuronidation or cytochrome P-450 levels. 4. Exposure of aniline-metabolizing hepatocytes to mersalyl, 2,2'-dithiodipyridine (DTP), 6,6'-carboxydipyridine disulphide (CPDS) or N-ethylmaleimide did not affect the biotransformation of aniline or cytochrome P-450 levels. 5. Metyrapone prevented degradation of cytochrome P-450. Exposure of cells to SKF-525 A inhibited aniline biotransformation without altering cytochrome P-450 levels. 6. PCMB and PCMBS inhibited aniline metabolism, probably by binding to a cysteinyl-SH residue in cytochrome P-450 apoenzyme and 'active sites' of UDP-glucuronyl transferases. Disulfiram inhibited aniline biotransformation, probably indirectly by diminishing NADPH.

antabuse loading dose 2015-07-14

During the past decade, significant advances have been made in the development of medications to treat alcohol dependence. Four medications have been approved by the U.S. Food and Drug Administration for treating alcohol dependence-naltrexone, injectable naltrexone, acamprosate, and disulfiram-and several others show promise. The fact remains, however, that because of the heterogeneity of alcohol dependence, these medications will not work for all people, in all circumstances. Moreover, clinicians are not routinely prescribing these medications for alcohol treatment. This commentary poses a number of issues that must be addressed in order to advance the alcohol research field and to make Depakote 7 Mg medications a mainstream treatment for problematic drinking. These issues are framed from the perspective of the various stakeholders involved, including clinicians, patients, regulatory agencies, the pharmaceutical industry, and third-party payers. Addressing these issues will not only help to improve treatment but, as further described, will also open up many new research opportunities for alcohol investigators in the coming decade.

antabuse online kopen 2017-06-22

Despite the success of combination antiretroviral therapy (cART), HIV persists in 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 Omnicef Uti Dosage , 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.