Disease relevance of Anticol

• The dose of DDP needed to eliminate the trypanosomes, 3 milligrams per kilogram of body weight per day for 7 days, was lethally toxic unless the animals received disulfiram orally and subcutaneous injections of physiologic saline, which reduced the acute renal necrosis caused by DDP alone [1].
• Letter: Disulfiram hypersensitivity hepatitis [2].
• Does disulfiram cure psoriasis [3].
• These results suggest that disulfiram has the potential to increase the efficacy of drug therapies for cancer and acquired immunodeficiency syndrome [4].
• Temazepam toxicity precipitated by disulfiram [5].

Psychiatry related information on Anticol

• Benefits of disulfiram use and CBT were most pronounced for participants who were not alcohol dependent at baseline or who fully abstained from drinking alcohol during treatment [6].
• 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 [7].
• As a functional corollary to alterations in neurochemical parameters, we observed significant disulfiram-induced increases in pain thresholds, potentiated by capsaicin treatment [8].
• Of 60 depressed alcoholics who completed an open trial of imipramine, 27 (45%) responded with improvement in both mood and drinking behavior, and eight (13%) responded after further dosage increases or treatment with disulfiram [9].
• Naltrexone and disulfiram in patients with alcohol dependence and comorbid post-traumatic stress disorder [10].

High impact information on Anticol

• Cure of mice infected with Trypanosoma rhodesiense by cis-diamminedichloroplatinum (II) and disulfiram rescue [1].
• Disulfiram hypersensitivity and rubber contact dermatitis [11].
• CONCLUSIONS: Disulfiram can potentially reduce P-gp-mediated drug resistance by inhibiting P-gp activity (possibly via cysteine modification) and/or by blocking its maturation [4].
• Blockage of drug resistance in vitro by disulfiram, a drug used to treat alcoholism [4].
• Half-maximal inhibition of ATPase activity occurred at 13.5 microM disulfiram [4].

Chemical compound and disease context of Anticol

• Since increased serum cholesterol is one of the risk factors in a coronary heart disease, chronic disulfirm therapy may increase the incidence of arteriosclerotic cardiovascular disease, as has been the case with chronic exposure to carbon disulfide, a principal metabolite of disulfiram [12].
• These observations offer an explanation for some of the previously reported neurological effects of disulfiram, such as its ability to prevent O2-induced seizures [13].
• Disulfiram and CS2 toxicity [14].
• Fulminant polyneuritis after overdose of disulfiram and ethanol [15].
• In B6 mice, we found that oral treatment with the aldehyde dehydrogenase (ALDH) inhibitor disulfiram decreased alcohol preference by 50%, whereas oral treatment of the catalase inhibitor 3-amino-1,2,4-triazole increased alcohol drinking preference by 15-20% [16].

Biological context of Anticol

• The usual phenotype was inhibited about 20%--30% by disulfiram and the unusual type up to 90% [17].
• Tetraethylthiuram disulfide at a level as low as 1 microgram/ml inhibited parasite glycolysis with no effect on glycolysis of normal erythrocytes [18].
• Moreover, the administration of disulfiram to neonatal mice decreased in vivo cell proliferation in the striatal SVZ [19].
• Dietary pretreatment of rats with disulfiram is known to prevent 1,2-dimethylhydrazine-induced colon carcinogenesis and was found to reduce DNA alkylation to less than 1% of that detected in animals treated with 1,2- di[14C]methylhydrazine alone [20].
• Using the alkaline elution technique to assay DNA damage, we found that disulfiram and diethyldithiocerbamate inhibited VP-16-induced single-strand breaks [21].

Anatomical context of Anticol

• Bisethylxanthogen, disulfiram, sodium diethyldithiocarbamate, and benzylisothiocyanate, administered at 0.5% of the diet (by weight) for 14 days, each induced significant increases in DT-diaphorase specific activities in cytosol fractions of lung, kidney, urinary bladder, proximal small intestine, and colon [22].
• Disulfiram-induced myocardial and skeletal-muscle degeneration in rats [23].
• 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 [7].
• With the use of a necrogenic dose of diethylnitrosamine and an assay for the carcinogen-induced early stages or resistant hepatocytes, the number of enzyme-altered foci was decreased to a major extent (up to 62%) by posttreatment with diethyldithiocarbamate, a derivative of disulfiram [24].
• Disulfiram did not deplete glutathione, and N-acetyl-L-cysteine could not prevent the effects of disulfiram on microtubules [25].

Associations of Anticol with other chemical compounds

• RESULTS: Disulfiram increased the sensitivity of P-gp-transfected cells to vinblastine and colchicine and inhibited P-gp's verapamil-stimulated ATPase activity [4].
• Thus, the mechanism by which daidzin suppresses ethanol intake in golden hamsters clearly differs from that proposed for the classic ALDH inhibitor disulfiram [26].
• These results indicate that (i) the action of daidzin differs from that proposed for the classic, broad-acting ALDH inhibitors (e.g., disulfiram), and (ii) the daidzin-sensitive mitochondrial ALDH is not the one and only enzyme that is essential for acetaldehyde metabolism in golden hamsters [27].
• Peptidylglycine alpha-amidating monooxygenase activity is dependent on copper, ascorbate, and molecular oxygen and is inhibited by the relatively selective copper chelator N,N-diethyldithiocarbamate or its disulfide dimer disulfiram (Antabuse) [8].
• Disulfiram administration affects substance P-like immunoreactive and monoaminergic neural systems in rodent brain [8].
• Although cimetidine had relatively small and variable effects on 2 subjects, disulfiram reduced skull radioactivity by about 70% and increased peak brain uptake by about 50% (n = 5) [28].

Gene context of Anticol

• Nevertheless, the specificity of single-dose disulfiram toward human CYP2E1 in vivo is unknown [29].
• In this study, we investigated the molecular and chemical basis of disulfiram as a multidrug resistance modulator [30].
• Finally, we have exploited MRP4 (ABCC4) to demonstrate that disulfiram can inhibit ATP binding by forming disulfide bonds between cysteines located in the vicinity of, although not in, the active site [30].
• METHODS: The involvement of CYP2E1 was assessed through pretreatment of adult human volunteers with disulfiram to inhibit the enzyme and the role of CYP3A4 through its induction in a second cohort of adults with rifampin (INN, rifampicin) [31].
• Identification of the human P-450 enzymes responsible for the sulfoxidation and thiono-oxidation of diethyldithiocarbamate methyl ester: role of P-450 enzymes in disulfiram bioactivation [32].

Analytical, diagnostic and therapeutic context of Anticol

• We conducted a controlled, blinded, multicenter study of disulfiram treatment of alcoholism in 605 men randomly assigned to 250 mg of disulfiram (202 men); 1 mg of disulfiram (204 men), a control for the threat of the disulfiram-ethanol reaction; or no disulfiram (199 men), a control for the counseling that all received [33].
• There were no apparent major differences between the results of tests run prior to the initiation of the disulfiram treatment and subsequent tests run up to 16 months after treatment was begun [34].
• None were treated with disulfiram or other medications during or after hospitalization [35].
• Conversely, oral administration of DSF lowered TNF-alpha serum level by 4-fold, lowered the delayed-type hypersensitivity response in a dose-dependent manner, and significantly inhibited adjuvant arthritis in Lewis rats [36].
• Using high-performance liquid chromatography, they found that a single 500-mg dose resulted in a gradual increase in plasma disulfiram and its metabolites, with peak levels generally occurring 8 hours after dosing [37].

References