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Experiments on rats were made to study the effect of alcohol and teturam on the function of spermatozoa and spermatogenesis of males and their progeny. The male-mediated damaging action of alcohol on the gonads of the progeny was ascertained. That might be one of the causes of the maldevelopment in subsequent generations of the progeny. Teturam was demonstrated to have an insignificant gonadotropic action and not to potentiate an adverse alcohol action on the male gonads.
1. The ability of alpha-methyl amino-acids and their corresponding amines to restore the sympathomimetic actions of tyramine, and the uptake of the amino-acids and the amines, were studied in isolated tissue preparations obtained from reserpine pretreated animals.2. Tyramine relaxed isolated rat ileum preparations from non-reserpinized rats but not from reserpine treated animals. alpha-Methyldopa, alpha-methylnoradrenaline and lower concentrations of metaraminol restored the responses of reserpinized preparations. alpha-Methyldopamine, alpha-methyl-m-tyrosine, alpha-methyl-p-tyrosine and higher concentrations of metaraminol did not do so. The restoring effect of alpha-methyldopa was blocked by disulphiram. alpha-Methyl-p-tyrosine or alpha-methyl-m-tyrosine blocked the restoring action of alpha-methyldopa but not of alpha-methylnoradrenaline. Cocaine blocked the restoration of responses to tyramine by alpha-methylnoradrenaline but not by alpha-methyldopa. alpha-Methyldopa and alpha-methylnoradrenaline failed to restore responses to tyramine in the presence of sodium-free Tyrode solution.3. Tyramine increased the perfusion pressure in isolated rabbit ear preparations obtained from non-reserpinized animals but was very much less active in preparations obtained from reserpine treated animals. alpha-Methyldopa, alpha-methyl-m-tyrosine, alpha-methylnoradrenaline, alpha-methyl-p-tyrosine and metaraminol restored the effects of tyramine. alpha-Methyldopamine did not do so. The restoring effect of alpha-methyldopa and alpha-methyl-m-tyrosine was blocked by disulfiram. alpha-Methyl-p-tyrosine blocked the restoring effect of alpha-methyl-m-tyrosine.4. Tyramine produced positive inotropic effects in isolated rabbit heart preparations. This was either reduced or absent in preparations obtained from reserpine pretreated animals. alpha-Methyldopa, alpha-methylnoradrenaline, alpha-methyl-m-tyrosine and metaraminol restored the responses to tyramine. alpha-Methyldopamine and alpha-methyl-p-tyrosine did not do so.
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Adherence to treatment decreased steadily with time (85.4% at 4 weeks, 36.6% at 16 weeks). Participants showed significant increases in percent abstinent days during treatment and at 24 weeks follow-up. Large reductions in anxiety, depression, and craving were observed during treatment, and improvement remained significant at 24 weeks. Duration of adherence with disulfiram strongly predicted abstinence at 16 weeks. There was no evidence of misuse of lorazepam or dose escalation during the study.
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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We studied the omega-oxidation of docosanoic acid (C22:0) in rat liver microsomes. C22:0 and 22-hydroxy-docosanoic acid (omega-hydroxy-C22:0) were used as substrates, and the reaction products were analyzed by electrospray ionization mass spectrometry. In the presence of NADPH, omega-oxidation of C22:0 produced not only the hydroxylated product, omega-hydroxy-C22:0, but also the dicarboxylic acid of C22:0, docosanedioic acid (C22:0-DCA). When rat liver microsomes were incubated with omega-hydroxy-C22:0 in the presence of either NAD+ or NADPH, C22:0-DCA was formed readily. Formation of C22:0-DCA from either C22:0 or omega-hydroxy-C22:0 with NADPH as cofactor was inhibited strongly by miconazole and disulfiram, whereas no inhibition was found with NAD+ as cofactor. Furthermore, omega-oxidation of C22:0 was reduced significantly when molecular oxygen was depleted. The high sensitivity toward the more specific cytochrome P450 inhibitors ketoconazole and 17-octadecynoic acid suggests that hydroxylation of C22:0 and omega-hydroxy-C22:0 may be catalyzed by one or more cytochrome P450 hydroxylases belonging to the CYP4A and/or CYP4F subfamily. This study demonstrates that C22:0 is a substrate for the omega-oxidation system in rat liver microsomes and that the product of the first hydroxylation step, omega-hydroxy-C22:0, may undergo further oxidation via two distinct pathways driven by NAD+ or NADPH.
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Despite growing interest in closing the "research to practice gap", there are few data on the availability of medications in American substance abuse treatment settings. Recent research suggests that organizational characteristics may be associated with medication availability. It is unclear if the availability of medications can be conceptualized in terms of "technology clusters", where the availability of a medication is positively associated with the likelihood that other medications are also offered. Using data from 403 privately funded and 363 publicly funded specialty substance abuse treatment centers in the US, this research models the availability of agonist medications, naltrexone, disulfiram, and SSRIs. Bivariate logistic regression models indicated considerable variation in adoption across publicly funded non-profit, government-owned, privately funded non-profit, and for-profit treatment centers. Some of these differences were attenuated by organizational characteristics, such as accreditation, the presence of staff physicians, and the availability of detoxification services. There was some evidence that naltrexone, disulfiram, and SSRIs represent a group of less intensely regulated medications that is distinct from more intensely regulated medications. These types of medications were associated with somewhat different correlates. Future research should continue to investigate the similarities and differences in the predictors of medication availability across national contexts.
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The QA process is recommended to anyone seeking to upgrade patient care delivery. It clarifies theories and gives substance to progressive ideas being considered for adoption. Certainly it tends to prevent premature and ill-conceived presentations. When an action is instituted, QA provides the framework that can be used to facilitate the change. As an afterthought, but as a welcome benefit, QA can foster teamwork and camaraderie among staff who assist in problem solving or bringing an idea to fruition.
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Previous studies suggested that a relative dopamine (DA) deficiency may explain the altered LH secretory dynamics that occur in patients with polycystic ovary syndrome (PCO). These studies included findings of decreased urinary excretion of homovanillic acid (HVA), a metabolite of DA, and increased urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG), the major brain metabolite of norepinephrine. To further explore the role of DA in these patients, disulfiram (250 mg) was administered daily for 2 weeks to alter the conversion of DA to norepinephrine and to increase both peripheral and central DA in patients with PCO and in normal women. LH pulse frequency and amplitude and the serum LH response to GnRH were assessed before and during disulfiram administration. A dopaminergic effect during disulfiram administration was evidenced by a decrease in serum PRL in the PCO patients and an increase in urinary HVA excretion and a decrease in the ratio of 3-methoxy-4-hydroxyphenylglycol to HVA in urine in both groups (all P less than 0.05). This increase in DA did not significantly alter the serum estrogen level, the mean serum LH level, LH pulse amplitude, or serum LH responses to GnRH in either the PCO patients or the normal women. These data suggest that increasing endogenous DA does not correct the inappropriate gonadotropin secretion characteristic of PCO and places further doubt on the importance of DA in explaining the altered LH secretory dynamics in these patients.
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The effects of carbon disulfide (CS2), diethyldithiocarbamate (DTC) and disulfiram (DS) on hepatic drug metabolism were studied in a noncirculating and hemoglobin-free rat liver perfusion system using p-nitroanisole (p-NA) as a substrate. Infusion of 1 mumol of CS2 into a normal rat liver instantaneously lowered the free p-nitrophenol (p-NP) concentration in the effluent perfusate; however, the effects on the levels of its glucuronide and sulfate conjugates were much less marked. The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups. Partial recovery was observed in the normal and PB-treated groups, but it was slow and slight in the 3-MC-treated group. Infusion of DTC, up to 20 mumol, did not lower free p-NP levels, but a slight transient increase was noted, especially in the 3-MC-group. Using 50 mumol of DTC, a slight suppression resulted. DS, up to 20 mumol, did not decrease p-NP production, but rather gradually increased it, especially in the 3-MC-treated groups. Without the p-NP infusion, about 60-70% of the infused DS (10 mumol) was recovered in the effluent perfusate as DTC plus its glucuronide conjugate, the formation of the latter being greatly enhanced by the inducer treatments and markedly suppressed during the p-NP infusion. In this paper, these results are discussed with regards to the mechanisms of drug metabolism inhibition by DS administration.
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The New England Veterans Integrated Service Network outpatient pharmacy files between January 1, 1998, and June 30, 2001, were analyzed; only patients with prescriptions on or after March 1, 1998, were included. Measurements for each patient included data on new and refilled prescriptions of disulfiram, naltrexone, and control medications. Prescription survival curves with right censoring were constructed. Distinct treatment episodes were defined by having six or more months between the end date of a prior prescription and the start date of a new prescription.
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Non-Small Cell Lung Cancer (NSCLC) is the most common type of lung cancer in both men and women. A recent phase IIb study demonstrated that disulfiram (DSF) in combination with cisplatin and vinorelbine was well tolerated and prolonged the survival of patients with newly diagnosed NSCLC. However, DSF is rapidly (4min) metabolised in the bloodstream and it is this issue which is limiting its anticancer application in the clinic. We have recently demonstrated that a low dose of DSF-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles supplemented with oral Cu inhibited tumour growth and reduced metastasis in a xenograft mouse lung cancer model. Here we demonstrate the influence of PLGA polymer, stabilizer loading and molecular weight as well as sonication time on the characteristics, including DSF release and the cytotoxicity of 10% w/w DSF-loaded PLGA nanoparticles. The paper demonstrates that the choice of PLGA as no significance on the characteristics of the nanoparticles apart from their DSF release, which is due to the differing degradation rates of the polymers. However, increasing the loading and molecular weight of the stabilizer as well as the sonication time reduced the size of the nanoparticles, reduced their ability to protect the DSF from reacting with Cu and degrading in serum, while increasing their DSF release rate and cytotoxicity. Additionally, increasing the sonication time resulted in the premature degradation of the PLGA, which increased the permeability of the nanoparticles further decreasing their ability to protect DSF from reacting with Cu and degrading in serum, while increasing their DSF release rate and cytotoxicity.
While antipsychotics remain the cornerstone of treatment for schizophrenic patients with comorbid substance use disorder (SUD), such treatment is nonetheless complicated by frequent medical comorbidity and poor adherence to medication.
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The authors describe a hypomanic-like reaction in a patient taking disulfiram and marijuana simultaneously and suggest there was an adverse interaction between the two drugs.
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Author describes development of the "Antabuse test" as preemployment predictive test of susceptibility of workers to carbon disulfide. He reviews all publications of his group, as well as publications of other groups on this subject. In discussion the hypothesis explaining this phenomenon is presented. Also practical suggestions for performing "Antabuse test" are mentioned.
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The present results demonstrate that the topical instillation of DSF eyedrops suppresses the inflammation in EIU, suggesting a possible novel approach for the treatment of ocular inflammation.
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The central concept was that of abstinence being a psychosocial construction, with the taking of disulfiram, being a physical manifestation of the decision not to drink. The main subthemes included the importance of participants believing in the potential for disulfiram producing a negative reaction, the increased autonomy achieved by disulfiram removing the need to ruminate on drinking decisions, and the importance of external structure, routine, and social contact with others to support ongoing engagement with disulfiram therapy.
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After traumatic injury to the central nervous system (CNS), various cytokines orchestrate the physiological responses of injured neurons and glial cells. The control of these intercellular signals is of major interest from a medical point of view. Since the transcriptional activator retinoic acid (RA) is known to regulate gene expression of cytokines in various cell culture systems we investigated the role of RA signaling in glial cells. The transcriptional activity of RA-induced genes is largely determined by the distribution of RA, which in turn depends on the local oxidation of retinaldehyde (RAL). This is synthesized from retinol or internalized as a component of vitamin A. Using high-pressure liquid chromatography and an RA-sensitive reporter cell line, we showed that OLN-93 cells, which serve as a model system for CNS oligodendrocytes, convert all-trans-RAL to the biologically active form all-trans-RA, but neither oxidize 9-cis-RAL nor isomerize RA enzymatically. The oligodendrocyte cell line expresses a cytosolic aldehyde dehydrogenase with an apparent molecular weight of 54-57 kDa and pI of 5.3-5.7. As indicated by a zymography bioassay, this enzyme is responsible for RA synthesis. The reaction requires NAD+ as cosubstrate and can be inhibited by disulfiram and citral. No other RA-producing enzyme activities were detected. These findings are in accordance with a putative role for retinoid signaling in neuroglial interactions in the CNS.
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Coprine, the disulfiram-like constituent of the mushroom Coprinus atramentarius was found to inhibit the low-Km dehydrogenase in rat liver and to increase the acetaldehyde level in blood during ethanol metabolism in vivo. Coprine did not inhibit the low-Km enzyme in vitro, but the hydrolytic product of coprine, 1-aminocyclo-propanol, was a potent inhibitor both in vitro and in vivo. A rapid onset of inhibition was observed after administration of coprine and the inhibition was long-lasting. It is suggested that 1-aminocyclopropanol is responsible for the inhibition caused by coprine in vivo.
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The physiological effects of disulfiram, in particular its adverse reaction when combined with alcohol, explains only part of its effect on problem drinking behaviour. The act of taking a disulfiram pill is also partly symbolic of making an absolute decision not to drink for a short period, allowing people with alcohol use disorder to explore other options for managing life without alcohol. Drug trials involving disulfiram need to treat it not simply as pharmaceutical but as part of a complex psychosocial intervention conducted within a supportive social context.
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DSF and RT combination therapy has additive therapeutic effects on AT/RT by potentiating programmed cell death, including apoptosis and autophagy of AT/RT cells. We suggest that DSF can be applied as a radiosensitizer in AT/RT treatment.
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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The threat of a disulfiram-ethanol reaction appears to affect cue reactivity physiologically rather than subjectively. While the data does not show changes in subjective ratings, it is possible that there are alternative beneficial effects arising from other cognitive processes that are not captivated by self-reported craving scales, reflected by decreases in negative affect and blood pressure. From this perspective, disulfiram might be recast to be more acceptable to patients.
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The objective of this study was to determine whether the thiol drug, diethyldithiocarbamate (DEDC) and its two metabolites, disulfiram (DS) and carbon disulfide (CS2) could be used as inhibitors of cytochrome P-450IIE1 to protect hepatocytes from cytotoxic xenobiotics. (1) Hepatocytes isolated from rats following pyrazole administration to induce cytochrome P-450IIE1 were much more susceptible to carbon tetrachloride (CCl4) and dimethylnitrosamine (DMN) than hepatocytes from untreated rats. Microsomes isolated from P-450IIE1-induced liver were also much more effective at catalysing a NADPH-dependent metabolism of CCl4 and DMN. The activities of aniline hydroxylase and p-nitroanisole-O-demethylase increased whereas ethoxyresorufin-O-dealkylase activity was much less induced and pentoxyresorufin-O-dealkylase activity was decreased. The P-450IIE1 antibody markedly inhibited the NADPH-dependent metabolism of these compounds indicating that IIE1 is a major catalyst of the microsomal metabolism of CCl4 and DMN. (2) Hepatocytes isolated from rats treated with DEDC or its metabolites, DS and CS2, on the other hand, were resistant to CCl4 and DMN. Microsomes isolated from the liver of animals treated with DEDC or DS or CS2 were also much less effective at catalysing the NADPH-dependent metabolism of the above compounds. DEDC markedly decreased the activities of aniline hydroxylase, p-nitroanisole-O-demethylase and pentoxyresorufin-O-dealkylase but had no effect on ethoxyresorufin-O-dealkylase activity. (3) Hepatocytes isolated from pyrazole-treated rats were also more susceptible to bromobenzene (BB) and naphthalene-induced cytotoxicity than hepatocytes from untreated rats. Furthermore, DEDC or CS2 administration beforehand significantly protected hepatocytes against both xenobiotics. (4) By contrast, hepatocytes isolated from P-450IIE1 induced rats were not more susceptible to lactonitrile or cyclophosphamide. Instead, cyclophosphamide was activated by phenobarbital-induced P-450 isozymes whereas lactonitrile was activated by alcohol dehydrogenase. Hepatocytes isolated from DEDC-treated rats were also resistant to cyclophosphamide but not lactonitrile. (5) The above results suggest that P-450IIE1 catalyses the cytotoxic activation of CCl4, DMN, BB and naphthalene but not of lactonitrile or cyclophosphamide. Furthermore, the administration of DEDC and its metabolites, disulfiram or CS2, inactivates P-450IIE1 so that the hepatocytes become resistant to these hepatotoxins.
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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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This work was carried out in order to evaluate the in vitro and in vivo toxicity of 3,4-dihydroxyphenylacetaldehyde (DOPAL). This aldehyde is formed from dopamine (DA) by monoamine oxidases (MAO) and is mainly oxidised to 3,4-dihydroxyphenylacetic acid by brain aldehyde dehydrogenases (ALDH), or eventually reduced to 3,4-dihydroxyphenylethanol by aldose/aldehyde reductases. In vitro, catecholaminergic SH-SY5Y cells were incubated with DA and disulfiram (DSF), an irreversible inhibitor of ALDH. As evidenced by MTT assays, a 24-h treatment with 10(-4) M DA and/or 10(-6) M DSF followed by a 24-h incubation in a drug-free medium evidenced that the toxicity of each of these drugs was potentiated by the second drug. HPLC measurements demonstrated that this drug association induced an early DOPAL production that could result in a delayed cell toxicity. For in vivo studies, male Sprague-Dawley rats were treated with L-DOPA-benserazide, which increases the production of DOPAL by MAO, and DSF. An acute injection of DSF (100mg/kg i.p.) and L-DOPA/benserazide (100mg/kg+25mg/kg, 24h later) significantly increased the DOPAL striatal level. However, a 30-day treatment with DSF (100mg/kg i.p., once every two days) and L-DOPA/benserazide (100mg/kg+25mg/kg, twice a day) did not affect both indexes used to assess the integrity of the nigro-striatal dopaminergic terminals (i.e. the striatal content in DA and the binding to the vesicular monoamine transporter on striatal membranes). These results do not support the hypothesis of a DOPAL toxicity and argue against the toxicity of L-DOPA therapy.
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A 49 year old female was started on disulfiram. Six weeks later she was given naproxen because of epicondylitis. After 5 days' treatment with naproxen she complained of nausea, anorexia and jaundice. At admission, bilirubin was 452 mumol/l, aspartate aminotransferase (ASAT) 1925 U/I, alanine aminotransferase (ALAT) 2815 U/I and prothrombin time measured as Normotest was 27%. The patient developed a fulminant hepatitis and died in hepatic coma almost four weeks after the introduction of naproxen. Postmortem examination disclosed a small liver (1,100 g) and histological examination showed massive necrosis and collapse of the lobules. The naproxen was the most probable cause of death, but it is impossible to exclude disulfiram as causative agent.
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The authors describe the clinical symptoms of a disulfiram overdose in a male patient and present the plasma concentrations of disulfiram and its metabolites 4 and 7 days after the overdose.
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Both inpatient and outpatient treatment centers that focus solely on psychosocial therapies for the treatment of alcohol dependence have high relapse rates. Thus, extensive research has focused on the development of pharmacologic moieties to attenuate the craving for alcohol after acute alcohol detoxification. Three drug therapies are currently approved by the US Food and Drug Administration (FDA) for this purpose: disulfiram, naltrexone, and acamprosate. The latter was approved by the FDA in 2004.
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Acute intentional overdoses of disulfiram (app. 30 g) is reported in 15-years-old boy. The neurological disturbances as nystagmus, coma, seizures and than impairment of memory and perception were dominated in the clinical picture. During MRI examination the areas of different signal from corpus callosum were detected which can be referred to focus of demyelinisation. The patient recovered and was discharged from the hospital after 30 days. Neuropsychological examinations have suggested dysfunction of CNS. The control MRI examination 90 days later, did not reveal any pathological changes in the brain.
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We reviewed the laboratory data of 408 alcoholics admitted for a 3 month course of alcohol detoxification and rehabilitation. Patients tested negative for hepatitis virus markers and were diagnosed as not having cirrhosis. Among the subjects, 222 patients received cyanamide treatment (a daily dose of 70 mg) without a history of disulfiram treatment, and 186 received disulfiram (a daily dose of 200 mg) without a history of cyanamide treatment. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels obtained at 0, 4, 8, and 12 weeks of administration of each aversive drug were compared between the two alcoholic groups.
It is well know that if an individual maintained on disulfiram (Antabuse) ingests alcohol, excess acetaldehyde is formed, resulting in a toxic reaction. In addition to this toxic interaction with alcohol (the basis of its use as a deterrent), there are both behavioral and biochemical observations to suggest that disulfiram alone has a direct effect on the CNS. The possibility that some of disulfiram's effects are related to alterations in biogenic amine metabolism led to the present study of cerebrospinal fluid amine metabolites in a group of male alcoholics. In this group, disulfiram treatment was associated with a significant reduction in homovanillic acid, the major metabolite of dopamine, while no change was noted in 5-hydroxyindoleacetic acid, the major metabolite of serotonin. Prior to disulfiram, patients with withdrawal symptoms had significantly lower homovanillic acid than those without such symptoms.
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Nickel allergy can result in both cutaneous and systemic manifestations, and can range from mild to severe symptoms. A severe form of this allergy is the Systemic nickel allergy syndrome, clinically characterized by cutaneous manifestions (contact dermatitis, pompholyx, hand dermatitis dyshydrosis, urticaria) with chronic course and systemic symptoms (headache, asthenia, itching, and gastrointestinal disorders related to histopathological alterations of gastrointestinal mucosa, borderline with celiac disease). This review aims to briefly update the reader on past and current therapies for nickel contact allergy.
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We propose that CYP2E1 activation occurs possibly due to OH* and contributes to H2O2-mediated LLC-PK1 cell necrosis by acting as a source of iron and perpetuating the generation of OH* via the Fenton reaction. Inhibition of CYP2E1 may be a novel approach for the prevention of tubular injury caused by oxidative stress.
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This study has demonstrated that cutaneous ADH and ALDH activities, located within defined subcellular compartments, play important roles in the activation and detoxification of CAlc and CAld in skin. Such findings are important to the development of computational hazard prediction tools for sensitisation (e.g. the DEREK program) and also to dermatologists in understanding observed interindividual differences, cross-reactivities or co-sensitisation to different cinnamic compounds in the clinic.
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The bacteriocolonic pathway for ethanol oxidation leads to high intracolonic levels of carcinogenic acetaldehyde. The respective roles of colonic mucosal cells and gut flora in the regulation of intracolonic acetaldehyde concentration are not known. Disulfiram inhibits hepatic acetaldehyde oxidation and may have an effect on colonic mucosal cells. On the other hand, metronidazole treatment leads to overgrowth of acetaldehyde-producing aerobic flora in the large intestine. The aim of this study was to characterize by means of disulfiram and metronidazole the contribution of colonic mucosal cells and intracolonic microbes to the regulation of intracolonic acetaldehyde concentration during ethanol oxidation in rats.
Substance use disorder is the most common psychiatric comorbidity in patients with schizophrenia, revealing prevalence rates of up to 65%. Recommendations of antipsychotic pharmacotherapy in schizophrenia are based on studies excluding patients with this double diagnosis. In this systematic review the available pharmacological studies in this subgroup of patients are summarised and discussed with regard to evidence-based medicine. Most available studies concern small sample sizes, and the level of evidence in those studies was low. Data suggest efficacy for second-generation antipsychotics (SGAs) (aripiprazole, clozapine, olanzapine, quetiapine, and risperidone) superior to orally administered conventional antipsychotics. Treatment with SGAs revealed superior improvement of distinct psychopathological symptoms, similarly to those studies excluding patients with comorbid substance abuse. In some studies reduced craving and increased reduction of substance abuse could be demonstrated. Tricyclic antidepressants (TCAs) added to antipsychotic maintenance therapy showed efficacy in reducing substance abuse and craving, whereas studies with other antidepressive agents (e.g. selective serotonin reuptake inhibitors) are lacking. Administration of the anti-craving agents naltrexone and disulfiram led to a decrease of drug intake in a few studies. Unfortunately no studies are available using acamprosate in patients with schizophrenia and comorbid alcoholism. In conclusion the preferential use of SGAs in patients with schizophrenia and comorbid substance use disorder is suggested, and the early initiation of concomitant treatment with TCAs (depending on current psychopathological status) and anti-craving agents has to be considered.