Disease relevance of aminomethanedithioic acid

• Ditiocarb sodium (diethyldithiocarbamate) therapy in patients with symptomatic HIV infection and AIDS. A randomized, double-blind, placebo-controlled, multicenter study [1].
• Prospective randomized trial of high-dose cisplatin and fluorouracil infusion with or without sodium diethyldithiocarbamate in recurrent and/or metastatic squamous cell carcinoma of the head and neck [2].
• Toxicity could be increased by the enzyme inhibitors L- and D-penicillamine, sodium diethyldithiocarbamate or 3-amino-1,2,4-triazole [3].
• 500 mg/kg sodium diethyldithiocarbamate (DDC) and trace quantities of uniformly labelled 14C-tyrosine were administered simultaneously to male albino rats of Porton-Wistar strain of approximately 210 g body weight [4].
• Radioprotective effect of sodium diethyldithiocarbamate (DDC) and S-2-aminoethyl-isothioronicadenosin-5-triphosphate (adeturon) in gamma-irradiated Escherichia coli cells [5].

High impact information on aminomethanedithioic acid

• Levamisole and sodium diethyldithiocarbamate can induce in vivo thymocyte differentiation from precursor spleen cells of nu/nu mice and evoke indirect plaque-forming cells in nude mice immunized with sheep red cells [6].
• Sodium diethyldithiocarbamate inducing long-lasting remission in case of juvenile systemic lupus erythematosus [7].
• The nephrotoxic effects of cis-dichlorodiamineplatinum(II) (NSC-119875) (DDP) in female F344 rats were effectively inhibited by administration of sodium diethyldithiocarbamate (DDTC) in doses of 750 mg/kg intraperitoneally or 100 mg/kg intravenously 2 hr after administration of DDP [8].
• By using the specific inhibitor of copper, zinc-containing SOD, sodium diethyldithiocarbamate (DDC), and the universal SOD inhibitor, sodium nitroprusside, we found that the predominant enzyme in guinea pig peritoneal MP is probably manganese-containing SOD [9].
• Antioxidant action of sodium diethyldithiocarbamate: reaction with hydrogen peroxide and superoxide radical [10].

Chemical compound and disease context of aminomethanedithioic acid

• Inhibitors of superoxide dismutase (sodium diethyldithiocarbamate) and catalase (hydroxyl amine and 3, amino 1,2,4-triazole) augmented Pf-II-mediated cutaneous photosensitization [11].
• The pulmonary toxicity of sodium diethyldithiocarbamate and lead(II) oxide alone or in combination was studied in rats after a single intratracheal instillation [12].
• Ethionamide, sodium diethyldithiocarbamate (Na-DDTC) and S-methyl diethyldithiocarbamate (Me-DDTC), three agents known to undergo metabolism by an S-oxidative pathway and diminish ANIT's toxicity, inhibited the in vitro enzymatic metabolism of ANIT by rat liver microsomes [13].
• In the lung--the principal target tissue for nickel carbonyl--a decrease was observed, and this may be the reason for the beneficial effect of sodium diethyldithiocarbamate in nickel carbonyl intoxications [14].

Biological context of aminomethanedithioic acid

• A dose-ranging pharmacokinetics study of sodium diethyldithiocarbamate in normal healthy volunteers [15].
• In mice exposed to 63Ni(CO)4 by inhalation, sodium diethyldithiocarbamate decreased the levels of the metal in tissues such as the lung, brain and heart [16].

Anatomical context of aminomethanedithioic acid

• Asymmetrical involvement of the cerebral neocortex on the response to an immunopotentiator, sodium diethyldithiocarbamate [17].
• We investigated whether sodium diethyldithiocarbamate (DETC), an inhibitor of the nuclear transcription factor kappa B (NFkappa B), modulates induction of NO synthase (NOS) in murine bone marrow-derived macrophages [18].
• Sodium diethyldithiocarbamate restores T lymphocyte proliferation, interleukin-2 production and NK activity in cyclophosphamide-immunosuppressed animals [19].
• Partial depletion and altered distribution of synaptic zinc in the rat hippocampus after treatment with sodium diethyldithiocarbamate [20].
• The inhibition of foam cell formation by sodium diethyldithiocarbamate [21].

Associations of aminomethanedithioic acid with other chemical compounds

• Here we report that the immunopotentiating activity of sodium diethyldithiocarbamate (Imuthiol), a compound that selectively increases T-cell numbers and activities, is dependent on an intact neocortex [17].
• Three Ni chelators were administered (1 mmol/kg, im) prior to injection of NiCl2 (0.25 mmol/kg, sc); d-penicillamine partially prevented Ni induction of renal heme oxygenase activity; triethylenetetramine had no effect; sodium diethyldithiocarbamate enhanced the Ni induction of renal heme oxygenase activity (three times greater than NiCl2 alone) [22].
• Greatest reduction of Po-210 in blood was achieved by 2,3-dimercaptopropanol (BAL), sodium diethyldithiocarbamate (DDTC), and N-(2,3-dimercaptopropyl) phthalamidic acid (DMPA) [23].
• Microsomal heme oxygenase activity was measured in liver and kidney of rats killed after administration of sodium diethyldithiocarbamate (DDC) and nickel chloride (NiCl2), singly and in combinations (DDC dosages: 0.33 to 1.33 mmol/kg, im, 17 hr before death; NiCl2 dosages: 0.125 and 0.25 mmol/kg, sc, 17 hr before death) [24].
• Disruption of central noradrenergic systems was achieved by (1) selective electrolytic lesion of noradrenergic cell bodies in the locus coeruleus or (2) administration of specific inhibitors of norepinephrine synthesis, sodium diethyldithiocarbamate (DDC) or 1-phenyl-3-(2-thiazolyl)-2 thiourea (U-14, 624) [25].

Gene context of aminomethanedithioic acid

• The methemoglobin formation in acatalasemic mice was also significantly inhibited by addition of more than 500 units/ml of catalase, and the methemoglobin formation in normal and acatalasemic mice was also inhibited with sodium diethyldithiocarbamate at a final concentration of 1 M [26].
• The influence of sodium diethyldithiocarbamate (DDC) on 63nickel chloride-induced metallothionein (MT) and alterations in essential metal levels in the liver of rats was investigated [27].
• Chromium(vi) can be determined directly by flow injection on-line sorbent extraction preconcentration coupled with electrothermal atomic absorption spectrometry using sodium diethyldithiocarbamate as the complexing agent and C18 bonded silica reversed-phase sorbent as the column material [28].
• During the first two months of observation, the patient was treated in succession with three chelating agents: 2,3-dimercapto-l-propanol (BAL), D-penicillamine and sodium diethyldithiocarbamate (Dithiocarb) [29].
• The synthesis of factors that monitor the expression of the Thy-1 cell surface component by marker-negative precursor cells requires an intact left cerebral cortex, whereas the activity of sodium diethyldithiocarbamate, an immunopotentiator that increases this synthesis, seems to require an intact right neocortex [30].

Analytical, diagnostic and therapeutic context of aminomethanedithioic acid

• A single injection with sodium diethyldithiocarbamate (SDEDTC, 1000 mg/kg i.p.) resulted within 1 h in a significant diminution of hippocampal (-23.9%) and cortical (-13.2%) zinc level, as revealed by atomic absorption spectrophotometry [20].
• Amelioration of type II collagen induced arthritis in rats by treatment with sodium diethyldithiocarbamate [31].
• The concentration of monohydrated compound was determined by liquid chromatography with post-column derivatization using sodium diethyldithiocarbamate as a reagent [32].
• Sodium diethyldithiocarbamate was active in increasing 63Ni2+ concentrations after both intravenous and oral administration [33].
• The effects of sodium diethyldithiocarbamate and DL-penicillamine on the fate of 63Ni2+ in mice injected with 63NiCl2 were studied by whole body autoradiography and liquid scintillation counting [34].

References