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The hypothesis that a quantity of noradrenaline released contingently on every response made to obtain brain stimulation mediates the reward produced by the stimulation was tested. An alternative hypothesis is that reward is mediated by a different system, but that a steady activation of post-synaptic receptors by noradrenaline is necessary for normal behavior. The synthesis of noradrenaline was inhibited by disulfiran, and when lateral hypothalamic self-stimulation in the rat had ceased, alpha-adrenergic stimulants were injected intraventricularly (IC) or intraperitoneally (IP). The directly acting receptor stimulants oxymetazoline (0.9-250 mug IC), naphazoline (20-250 mug IC), and clonidine (0.75-3 mug IC, 0.037-3 mg/kg IP) did not restore self-stimulation, but the indirectly acting stimulants amphetamine (2 mg/kg IP), methylphenidate (3 mg/kg IP) and phenylephrine (15 mug IC) did not restore self-stimulation. In Experiments 2 and 3, in which either the functional noradrenaline pool was depleted with disulfiram and amphetamine, or the reserve noradrenaline pool was depleted with reserpine, the action of phenylephrine in restoring self-stimulation was shown to be indirect, probably by mobilizing a reserve pool of noradrenaline. Because only indirectly acting noradrenergic stimulants which facilitate the release of noradrenaline restores self-stimulation, it is concluded that noradrenaline must be released contingent on every response for self-stimulation to occur. Whether this released noradrenaline mediates the reward or has some other function associated with bar-pressing behavior remains to be shown.
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We examined the effects of Dbh gene dosage and the DBH inhibitor disulfiram in mice with zero, one, or two null Dbh alleles (+/+, +/-, and-/- mice).
In recent years, advances in neuroscience led to the development of new medications to treat alcohol dependence and especially to prevent alcohol relapse after detoxification. Whereas the earliest medications against alcohol dependence were fortuitously discovered, recently developed drugs are increasingly based on alcohol's neurobiological mechanisms of action. This review discusses the most recent developments in alcohol pharmacotherapy and emphasizes the neurobiological basis of anti-alcohol medications. There are currently three approved drugs for the treatment of alcohol dependence with quite different mechanisms of action. Disulfiram is an inhibitor of the enzyme aldehyde dehydrogenase and acts as an alcohol-deterrent drug. Naltrexone, an opiate antagonist, reduces alcohol craving and relapse in heavy drinking, probably via a modulation of the mesolimbic dopamine activity. Finally, acamprosate helps maintaining alcohol abstinence, probably through a normalization of the chronic alcohol-induced hyperglutamatergic state. In addition to these approved medications, many other drugs have been suggested for preventing alcohol consumption on the basis of preclinical studies. Some of these drugs remain promising, whereas others have produced disappointing results in preliminary clinical studies. These new drugs in the field of alcohol pharmacotherapy are also discussed, together with their mechanisms of action.
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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 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.
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Disulfiram (DSF), a treatment for alcohol use disorders, has shown some clinical effectiveness in treating addiction to cocaine, nicotine, and pathological gambling. The mechanism of action of DSF for treating these addictions is unclear but it is unlikely to involve the inhibition of liver aldehyde dehydrogenase (ALDH2). DSF is a pro-drug and forms a number of metabolites, one of which is N-acetyl-S-(N,N-diethylcarbamoyl) cysteine (DETC-NAC). Here we describe a LCMS/MS method on a QQQ type instrument to quantify DETC-NAC in plasma and intracellular fluid from mammalian brain. An internal standard, the N,N-di-isopropylcarbamoyl homolog (MIM: 291>128) is easily separable from DETC-NAC (MIM: 263>100) on C18 RP media with a methanol gradient. The method's linear range is 0.5-500 nM from plasma and dialysate salt solution with all precisions better than 10% RSD. DETC-NAC and internal standards were recovered at better than 95% from all matrices, perchloric acid precipitation (plasma) or formic acid addition (salt) and is stable in plasma or salt at low pH for up to 24 h. Stability is observed through three freeze-thaw cycles per day for 7 days. No HPLC peak area matrix effect was greater than 10%. A human plasma sample from a prior analysis for S-(N,N-diethylcarbamoyl) glutathione (CARB) was found to have DETC NAC as well. In other human plasma samples from 62.5 mg/d and 250 mg/d dosing, CARB concentration peaks at 0.3 and 4 nM at 3 h followed by DETC-NAC peaks of 11 and 70 nM 2 h later. Employing microdialysis sampling, DETC-NAC levels in the nucleus accumbens (NAc), medial prefrontal cortex (mPFC), and plasma of rats treated with DSF reached 1.1, 2.5 and 80 nM at 6h. The correlation between the appearance and long duration of DETC-NAC concentration in rat brain and the persistence of DSF-induced changes in neurotransmitters observed by Faiman et al. (Neuropharmacology, 2013, 75C, 95-105) is discussed.
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DBH protein levels in adrenal and prefrontal cortex (PFC) and adrenal DBH activity were proportional to number of wild-type alleles. Adrenal DA was slightly increased in+/- mice and markedly increased (80-fold) in -/- mice compared to wild-type animals. While adrenal NE and epinephrine (EPI) were undetectable in -/- mice, adrenal concentrations of NE and EPI were similar in +/+ and +/- mice, suggesting that the increase in DA maintains the normal rate of beta-hydroxylation in Dbh +/- mice. Disulfiram had little effect on adrenal catecholamine levels, regardless of genotype or dose. NE was absent in the PFC of -/- mice, but only slightly reduced in +/- animals compared to wild-type animals. PFC DA was increased twofold in +/- mice and fivefold in -/- mice, and the NE to DA ratio was reduced ( approximately 35%) in +/- mice, compared to wild-type mice. Disulfiram significantly decreased PFC NE and increased DA in +/+ and +/- animals, with the disulfiram and genotype effects on the PFC NE to DA ratio apparently additive.
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The aim of this study was to assess the effectiveness, tolerability, and safety of alcohol relapse prevention with disulfiram in alcohol-dependent patients in opioid maintenance treatment under routine treatment conditions.
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Since Chevens' report, in the early 50's that his patients under treatment with the aldehyde dehydrogenase inhibitor, antabuse, could experience beneficial effects when drinking small volumes of alcoholic beverages, the role of acetaldehyde (ACD) in the effects of ethanol has been thoroughly investigated on pre-clinical grounds. Thus, after more than 25 years of intense research, a large number of studies have been published on the motivational properties of ACD itself as well as on the role that ethanol-derived ACD plays in the effects of ethanol. Accordingly, in particular with respect to the motivational properties of ethanol, these studies were developed following two main strategies: on one hand, were aimed to challenge the suggestion that also ACD may exert motivational properties on its own, while, on the other, with the aid of enzymatic manipulations or ACD inactivation, were aimed to test the hypothesis that ethanol-derived ACD might have a role in ethanol motivational effects. Furthermore, recent evidence significantly contributed to highlight, as possible mechanisms of action of ACD, its ability to commit either dopaminergic and opioidergic transmission as well as to activate the Extracellular signal Regulated Kinase cascade transduction pathway in reward-related brain structures. In conclusion, and despite the observation that ACD seems also to have inherited the elusive nature of its parent compound, the behavioral and biochemical evidence reviewed points to ACD as a neuroactive molecule able, on its own and as ethanol metabolite, to exert motivational effects.
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Freshly obtained human term placentae were subjected to subcellular fractionation to study the localization of NAD-dependent aldehyde dehydrogenases. Optimal conditions for the cross-contamination-free subcellular fractionation were standardized as judged by the presence or the absence of appropriate marker enzymes. Two distinct isozymes, aldehyde dehydrogenase I and II, were detected in placental extracts after isoelectric focusing on polyacrylamide gels. Based on a placental wet weight, about 80% of the total aldehyde dehydrogenase activity was found in the cytosolic acid and about 10% in the mitochondrial fraction. The soluble fraction (cytosol) contained predominantly aldehyde dehydrogenase II which has a relatively high Km (9 mmol/l) for acetaldehyde and is strongly inhibited by disulfiram. The results indicate that cytosol is the main site for acetaldehyde oxidation, but the enzyme activity is too slow to prevent the placental passage of normal concentrations of blood acetaldehyde (less than 1 mumol/l) produced by maternal ethanol metabolism.
Disulfiram is used 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.
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The significance of toxic neuropathy is shown by the fact that the recognition of clinical picture, identifying etiological factors and its elimination may prevent the evolution of polyneuropathy. This allows for more effective treatment of these neuropathies as apposite to idiopathic ones which can be treated only symptomatically. Our case report indicates the possibilities during a period with no serious damage to the axons manifested.
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Acamprosate (calcium acetylhomotaurinate), a synthetic compound with a similar chemical structure to that of gamma-aminobutyric acid, is thought to act via several mechanisms affecting multiple neurotransmitter systems; inhibition of neuronal hyperexcitability by antagonism of excitatory amino acid activity and reduction of calcium ion fluxes has been suggested as its predominant mechanism of action. The drug is the first agent specifically designed to maintain abstinence in alcohol (ethanol)-dependent patients after detoxification. Voluntary oral ethanol consumption in ethanol-preferring or ethanol-dependent rats is dose-dependently reduced by acamprosate: total fluid intake and food consumption are not affected. The drug does not potentiate the acute or chronic toxic effects of ethanol and has no hypnotic, antidepressant, anxiolytic or muscle-relaxant effects in animals. There is no evidence of abuse potential with acamprosate. Oral acamprosate 1.3 or 2 g/day in 3 divided doses administered for 3 to 12 months to alcohol-dependent patients after detoxification was more effective than placebo in preventing alcohol relapse according to abstinence rates, duration of abstinence, gamma-glutamyl transferase levels and/or a variety of other clinical or biological end-points. Concomitant psychosocial/behavioural therapies were used in some trials. Compared with those with placebo, the superior abstinence rates and durations of abstinence with acamprosate were maintained during 6- to 12-month post-treatment follow-up periods, and greater abstinence rates with acamprosate were confirmed in a pooled analysis of data from 11 randomised placebo-controlled trials involving a total of 3338 patients with alcohol dependence. The efficacy of acamprosate appears to be dose dependent and enhanced by the addition of disulfiram. Acamprosate was generally well tolerated in placebo-controlled trials. The most common adverse events were gastrointestinal (especially diarrhoea) or dermatological and were mostly mild and transient. The percentage of patient withdrawals because of adverse events was similar in acamprosate and placebo groups. No trials have compared the efficacy or tolerability of acamprosate with those of other treatment approaches (including opiate antagonists or selective serotonin reuptake inhibitors) aimed at maintaining abstinence in detoxified alcohol-dependent patients. Thus, acamprosate, as an adjunct to psychosocial/behavioural therapies, represents a novel advance for the management of alcohol-dependent patients in the postdetoxification period. Longer term and comparative trials with other active therapies are required to confirm these promising results.
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In vitro experiments with human liver microsomes showed the cyanide concentration was significantly lower after incubation with acetonitrile and disulfiram than acetonitrile alone (a mean 60% reduction in cyanide level).
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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, 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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To investigate the possible disulfiram-like properties of metronidazole and ethanol in human volunteers.
Cancer stem cells (CSCs) are thought to be at the root of cancer recurrence because they resist conventional therapies and subsequently reinitiate tumor cell growth. Thus, targeting CSCs could be the bullseye to successful cancer therapeutics in the future. Brain tumors are some of the most challenging types of cancer to treat and the median survival following the initial diagnosis is 12-18 months. Among the different types of brain tumors, glioblastoma (GBM) is considered the most aggressive and remains extremely difficult to treat. Despite surgery, radiation, and chemotherapy, most patients develop refractory disease. Temozolomide (TMZ) is a chemotherapy used to treat GBM however resistance develops in most patients. The underlying mechanisms for TMZ resistance (TMZ-resistant) involve the expression of DNA repair gene O(6)-methylguanine-DNA methyltransferase. CSC genes such as Sox-2, BMI-1, and more recently Y-box binding protein-1 also play a role in resistance. In order to develop novel therapies for GBM, libraries of small interfering RNAs and off-patent drugs have been screened. Over the past few years, several independent laboratories identified disulfiram (DSF) as an off-patent drug that kills GBM CSCs. Reportedly DSF has several modes of action including its ability to inhibit aldehyde dehydrogenases, E3 ligase, polo-like kinase 1, and NFkB. Due to the fact that GBM is a disease of heterogeneity, chemotherapy with multitargeting properties may be the way of the future. In broader terms, DSF kills CSCs from a range of different cancer types further supporting the idea of repurposing it for "target practice."
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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.
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There is an emerging trend to restudy known drugs for their anti-cancer potential. One such anti-alcoholic drug, disulfiram, with significant anti-cancer potential was studied for its efficacy against Hep3B cell lines, an in vitro model of hepatocellular carcinoma. Simultaneously, we intended to study the effect of polysorbate 80-stabilized PLGA nanoparticles and its DSF-loaded counterpart. Cell and nuclear staining, comet assay, flow cytometry and Western blots were performed. Results suggest that cell proliferation was inhibited by DSF and its PLGA nanoparticles through cell cycle arrest, triggering activation of apoptotic pathways that culminates with cell death. DSF loaded nanoparticles when compared with free DSF, showed significantly lesser effect due to its sustained drug-releasing property, while empty nanoparticles showed negligible influence on Hep3B cells. Our results suggest that DSF alone contributes to cell death, while polysorbate 80-stabilized PLGA nanoparticles show sustained drug release patterns that would potentially lower dosage regimens.
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MVA-B was safe and well tolerated. A minor, but significant, increase in the T cell responses targeting vaccine inserts of Gag was observed [a median of 290, 403 and 435 spot-forming-cells/10(6) PBMCs at baseline, after two vaccinations and after three vaccinations, respectively; P = 0.02 and P = 0.04]. After interruption of cART, a modest delay in the rebound of the plasma viral load in participants receiving vaccine but not disulfiram was observed compared with placebo recipients (P = 0.01). The dynamics of the viral load rebound did not change in patients receiving MVA-B/disulfiram. No changes in the proviral reservoir were observed after disulfiram treatment.
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Pyrazole, previously reported to inhibit ethanol oxidation in the rat, also effectively blocks the in vivo metabolism of methanol, propanol, isopropanol, n-butanol, and isobutanol. A variety of oximes and amides are also effective inhibitors of ethanol metabolism. These various inhibitors may prove important in the elucidation of several facets of alcohol metabolism and also may have application in the treatment of methanol poisoning and in the reduction of the sequelae of the disulfiram-ethanol reaction syndrome in man.
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A patient was brought into the emergency ward with a suspected alcohol intoxication. As it turned out, she had experienced a severe disulfiram-ethanol reaction which had led to hypotensive shock; extensive abnormalities were seen on the ECG. The patient was admitted to the intensive care unit. High-dose norepinephrine treatment was needed to bring the blood pressure back to normal. The use of disulfiram was only discovered at a later stage.
A 53-year-old client with a history of alcohol and amineptine misuse and a long history of recurrent depression, for which he was prescribed venlafaxine tablets. Over time, he increased the dosage to 50 tablets daily (3750 mg). Large venlafaxine dosages produced amphetamine-like effects, due possibly to the related increase in dopamine turnover. Once hospitalized for detoxification, the patient had a symptomatology which was consistent with a serotonergic discontinuation syndrome.
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Most patients presented with somatic and/or psychiatric comorbidity and/or polydrug use at baseline. Half of the patients completed 6 months of disulfiram treatment. Alcohol use was low during disulfiram treatment. Levels of other drug use did not change. For most patients, 1 or more adverse events were reported, often mild and/or short lived. Three patients experienced severe adverse events attributable to disulfiram.
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Twenty-nine opioid maintenance treatment patients were observed from the beginning of outpatient disulfiram treatment for up to 6 months. Patients received disulfiram (mostly 300 mg/d) together with their daily opioid dose. Patients were assessed through urine screens for alcohol (ethyl gluconoride) and other drugs at least twice monthly; blood chemistry analyses after 1, 3, and 6 months; and clinical interviews after 3 and 6 months.
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The radiation modifying effect and toxicity of tetraethylthiuram disulfide (disulfiram) have been studied. Disulfiram (DSM) inhibits aldehyde dehydrogenase, dopamine-beta-oxygenase, microsomal mixed-function oxidases and cytochrome P-450 enzymes. It is widely used for aversion therapy in alcoholism. Disulfiram also inhibits tumor formation by several known carcinogens. A biphasic toxicity pattern of DSM is reported in the L-929 mouse fibroblast culture system. Disulfiram is 100 percent toxic at 2 X 10(-7) M (0.05 micrograms per ml), 23 percent toxic at 3 X 10(-7) M (0.1 microgram per ml), and 100 percent toxic again at 3.4 X 10(-6) M (1.0 microgram per ml). The pattern is similar to the biphasic toxicity pattern of DMS's major metabolite, sodium diethyldithiocarbamate (DTC). Reports of both radiation protection and radiation enhancement by DTC exist. Previously, a radioprotective effect by 2 X 10(-6) M DTC (dose modifying factor = 1.26) has been demonstrated in the L-929 cell system. To date, no radiation modifying properties of DSM have been reported. Our investigation of DSM as a radiation modifier at 3 X 10(-7) M (0.1 microgram per ml) did not show significant improvement in survival of irradiated cells treated with DSM relative to the irradiated control group, as determined by absence of a difference in the Do of the two groups. Considering DSM's close structural relationship to DTC, it is possible that DSM may exhibit a radioprotective effect when applied in a different concentration than what was used in our research.
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The benefits of selective serotonin reuptake inhibitors, disulfiram, and lithium have not been clear for people with alcohol dependence. While the results of many studies have suggested that opioid agonists increase alcohol consumption, others have shown that mu-opioid antagonists and partial agonists reduce alcohol consumption. The results from animal studies suggest that these agents may prevent the reinforcing effects of alcohol consumption. Based on the results of those animal studies, some opioid antagonists, such as, naltrexone, nalmefene, have been studied for their benefits in treating alcohol dependence.
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Avian tibial dyschondroplasia is a disease found in fast growing strains of chickens, ducks, and turkeys worldwide in which growth plate cartilage accumulates in the metaphyseal region of the tibiotarsus; it is similar to mammalian osteochondrosis. Several biochemical and pathologic studies have shown that the growth plate chondrocytes do not reach their expected size in the hypertrophic zone and necroses prematurely. The chondrocytes also produce decreased amounts of extracellular proteins, such as collagen X and fibroblast growth factor-beta, that are necessary for cartilage maturation. This immature cartilage becomes highly cross-linked in the collagen molecules and apparently resistant to resorption and vascularization by the metaphyseal vessels. The dyschondroplastic cartilage remains in the metaphysis for several weeks. Not until the growth rate of the birds slows down is the cartilage able to be resorbed and replaced by trabecular bone. Many conditions have been found to induce tibial dyschondroplasia, including copper deficiency; fusarochromanone, thiram, and antabuse intoxication; excessive dietary levels of cysteine and homocysteine; metabolic acidosis; and bird rearing environment. However, the mechanism(s) by which these various methods induce tibial dyschondroplasia is presently not known. Current research is focusing on understanding the development of the disease and whether or not all these methods work by the same physiological chain of events. Recent biochemical evidence suggests that a copper deficiency might be caused by a different mechanism than genetically and thiram-induced tibial dyschondroplasia.
Oral treatment of rats with tetramethylthiuram disulphide (TMTDS), 0.1% mixed in the food (corresponding to 20--30 mumol daily) for one week, increased the brain levels of endogenous copper and zinc to 120% and 170%, respectively, of the control levels. Mice injected with HgCl2 (2.5 mumol/kg) were used to study further the effect of DDC (diethyldithiocarbamate), disulfiram, TMTDS or CS2 on heavy metal distribution. The brain levels of Hg were significantly increased in mice given DDC or TMTDS. Disulfiram and CS2 increased the brain levels marginally. Pregnant rats exposed to HgCl2 (0.5 mumol/kg) were also included in the studies. Treatment with DDC (0.5 mmol/kg) immediately after the mercury injection, increased the maternal brain concentration of mercury considerably, as measured after 24 and 78 h. The kidney levels were also increased. In the foetuses, the brain and liver levels were transiently increased after treatment with diethyldithiocarbamate. The observations support the hypothesis that the neurotoxicity of diethyldithiocarbamate and other thiocarbamates may be related to changes in heavy metal metabolism.
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The initial purpose of the study was to determine the potential of acetaldehyde (Ace) to increase the rate of sister-chromatid exchanges (SCEs) in mouse spermatogonia. We tested four doses of Ace (from 0.4 to 400.0 mg/kg), including a negative and a positive control group (distilled water and cyclophosphamide, respectively). The results showed that all tested doses were SCE inducers. The highest tested dose increased the control level more than three times. Also, the cumulative frequencies of SCEs per cell were higher in the Ace-treated animals than in the control cells. Ace is transformed into acetate through the enzyme aldehyde dehydrogenase, a process that may be blocked by disulfiram (Dis) generating the accumulation of Ace. The second purpose of the study was to determine if the administration of Dis (150 mg/kg) could increase the SCE rate produced by non-genotoxic doses of Ace. (0.004 and 0.04 mg/kg). The animals treated with the two doses of Ace alone showed no increase in the frequency of SCEs; also, Dis by itself was not an SCE inducer. However, the groups of animals previously treated with Dis showed an increase of 31 and 60% with respect to the values obtained with the two doses of Ace alone. Furthermore, the cumulative frequencies of SCEs per cell were higher in the animals administered with both compounds together than in those treated with them separately. These results suggest the need to extend this type of study to other models.
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NTX at the dose of 50 mg/day is effective for alcohol dependence in short-term treatment. The optimal duration of NTX treatment may be longer than 3 months. The evidence so far may be too little to support the superiority of NTX to acamprosate and the inferiority of NTX to disulfiram. NTX treatment should be concurrently given with a psychosocial intervention. Other patterns of NTX administration should not be used at present, e.g., a dose of three times a week, combined NTX with other biological treatments. NMF has no role for the treatment of alcohol dependence in clinical practice. Randomised, double-blind, placebo-controlled trials of NTX treatment in patients with alcohol dependence are still needed. Some issues should be concerned in further studies. Firstly, further trials should be conducted in larger sample sizes and over longer periods of time. Secondly, other than the outcomes relevant to alcohol use, some important outcomes should also be measured, e.g., functioning, health-related quality of life, economic cost. Thirdly, the comparisons between NTX and other treatments for alcohol dependence, both biological and psychosocial, should be investigated. Fourthly, combined treatments of NTX and other biological treatments for alcohol dependence may be in issue of interest. Lastly, high discontinuation rate in both treatment and control groups should be concerned.
The aim of the present study was firstly to describe the characteristics of alcoholic outpatients (A) suffering from co-morbid personality disorder (PD) of either the cluster B (A+PDB) or cluster C (A+PDC) type. Secondly, to investigate the effect of various kinds of treatment to be able to single out the most beneficial therapy. Thirdly, to identify the most beneficial treatment. The patients were offered the following outpatient treatments: cognitive behaviour therapy, family therapy and supportive consultations. The material consisted of 363 patients who started psychosocial treatment at the outpatient alcohol clinic at Odense University Hospital, Denmark. It was possible to re-interview 276 (76%) patients 1 year after onset of treatment. Of the 363 patients, 87% were alcohol-dependent (ICD-10) and 34% fulfilled the ICD-10-R criteria for PDs. The basic interviews focused on the seven main areas of the Addiction Severity Index. A+PDC had significantly more serious medical problems than A-PD, while the A+PDB group had significantly more employment, drug use and social problems than the A-PD. As for psychiatric status, A-PD had significantly different scores compared with A+PDB and A+PDC. A+PDB were younger and had a longer history of alcohol abuse than A-PD and A+PDC. After treatment there was no significance between the patients with and without PD concerning alcohol outcome and psychosocial outcome. The significance of co-morbid PD for the prognosis of alcohol abusers may be overestimated. Our results indicate that A+PD can be treated as successfully as other patients in an outpatient alcohol clinic can.
During forensic examination of male fertility in disputed paternity cases cheating is possible. There are substances with effects on spermatogenesis; on transport of spermatozoa and on hormonic regulation. Bis-dichloroacetyl-octamethylendiamine seems the most suitable. It has no side-effects, exept for an antabuse-effect. By daily treatment with 200 mg sterility starts after 2--3 months. After stopping the treatment fertility becomes normal after 2 months.