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SODIUM DIMETHYLDITHIOCARBAMATE HYDRATE - CAS 207233-95-2

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Category
Main Product
Product Name
SODIUM DIMETHYLDITHIOCARBAMATE HYDRATE
Catalog Number
207233-95-2
Synonyms
sodium; N,N-dimethylcarbamodithioate; hydrate; Sodiumdimethyldithiocarbamatehydrate; 207233-95-2; Dimethyldithiocarbamicacidsodiumsalt
CAS Number
207233-95-2
Molecular Weight
143.21
Molecular Formula
C3H6NNaS2·1/2H2O
COA
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MSDS
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Canonical SMILES
CN(C)C(=S)[S-].O.[Na+]
InChI
InChI=1S/C3H7NS2.Na.H2O/c1-4(2)3(5)6;;/h1-2H3,(H,5,6);;1H2/q;+1;/p-1
InChIKey
RJCVAPZBRKHUSV-UHFFFAOYSA-M
Structure
CAS 207233-95-2 SODIUM DIMETHYLDITHIOCARBAMATE HYDRATE
Specification
Purity
95%
Melting Point
120-122ºC (dec.)(lit.)
Reference Reading
1.Further studies of the action of disulfiram and 2,2'-dithiodipyridine on the dehydrogenase and esterase activities of sheep liver cytoplasmic aldehyde dehydrogenase.
Kitson TM. Biochem J. 1982 Jun 1;203(3):743-54.
1. Pre-modification of cytoplasmic aldehyde dehydrogenase by disulfiram results in the same extent of inactivation when the enzyme is subsequently assayed as a dehydrogenase or as an esterase. 2. 4-Nitrophenyl acetate protects the enzyme against inactivation by disulfiram, particularly well in the absence of NAD+. Some protection is also provided by chloral hydrate and indol-3-ylacetaldehyde (in the absence of NAD+). 3. When disulfiram is prevented from reacting at its usual site by the presence of 4-nitrophenyl acetate, it reacts elsewhere on the enzyme molecule without causing inactivation. 4. Enzyme in the presence of aldehyde and NAD+ is not at all protected against disulfiram. It is proposed that, under these circumstances, disulfiram reacts with the enzyme-NADH complex formed in the enzyme-catalysed reaction. 5. Modification by disulfiram results in a decrease in the amplitude of the burst of NADH formation during the dehydrogenase reaction, as well as a decrease in the steady-state rate.
2.Suppressing glioblastoma stem cell function by aldehyde dehydrogenase inhibition with chloramphenicol or disulfiram as a new treatment adjunct: an hypothesis.
Kast RE1, Belda-Iniesta C. Curr Stem Cell Res Ther. 2009 Dec;4(4):314-7.
Strong expression of aldehyde dehydrogenase is a prominent feature of both normal and cancer stem cells, including the stem cell sub-population of glioblastoma. Aldehyde dehydrogenase function is used by cancer stem cells to repopulate a tumor mass after chemotherapy cytoreduction. Cancer stem cells tend to be chemotherapy compared to the non-stem cell majority cell population in several common human cancers. Such has been demonstrated specifically in glioblastoma. In normal hematopoietic stem cells with unimpaired high levels of aldehyde dehydrogenase, stem cells divide rarely and then asymmetrically to a daughter stem cell and a daughter cell on a path of differentiation or symmetrically with both daughter cells on a differentiated path. If a parallel situation obtains in glioblastoma stem cells, the migrating, far flung paucicellular extensions will be stem cell rich and use aldehyde dehydrogenase to generate the characteristic multiple metastases made up of mostly non-stem cells.
3.Disulfiram neuropathy: a review (1971-1988) and report of a case.
Frisoni GB1, Di Monda V. Alcohol Alcohol. 1989;24(5):429-37.
Neuropathy is one of the most severe side effects of disulfiram therapy. We report the case of a young man who developed a neuropathy following disulfiram administration, with a virtually complete recovery in 14 months. We then discuss 37 cases of disulfiram neuropathy reported since 1971. Evidence is given that: (1) there is no numerical sex prevalence, although the incidence of the disease in women is probably disproportionately high; (2) symptom onset latency is dose-dependent, being longer at 250 mg/day or less; (3) neurological deficits are also dose-dependent, being milder at 250 mg/day or less; (4) the two previous findings and single observations suggest that disulfiram neuropathy is a dose-dependent phenomenon; (5) recovery probably follows a course which depends primarily on the initial degree of impairment; (6) the genetic mechanism probably involves carbon disulfide and a hypothesis as to the possible biochemical mechanism is proposed; (7) chloral hydrate can bear a potentiation effect on neuropathy, and the association with disulfiram is best avoided.
4.Hydrogen peroxide yields during the incompatible interaction of tobacco suspension cells inoculated with Phytophthora nicotianae.
Able AJ1, Guest DI, Sutherland MW. Plant Physiol. 2000 Oct;124(2):899-910.
Rates of H(2)O(2) production by tobacco suspension cells inoculated with zoospores from compatible or incompatible races of the pathogen Phytophthora nicotianae were followed by direct measurement of oxygen evolution from culture supernatants following catalase addition. Rates of HO(2)(*)/O(2)(-) production were compared by following the formation of the formazan of sodium, 3'-[1-[phenylamino-carbonyl]-3,4-tetrazolium]-bis(4-methoxy-6-nitro) benzene-sulfonic acid hydrate. In the incompatible interaction only, both reactive oxygen species (ROS) were produced by the cultured host cells in a minor burst between 0 and 2 h and then in a major burst between 8 and 12 h after inoculation. Absolute levels of H(2)O(2) could not be accurately measured due to its metabolism by host cells, but results are consistent with the majority of H(2)O(2) being formed via dismutation of HO(2)(*)/O(2)(-). The effects of inhibitors of endogenous Cu/Zn superoxide dismutase (diethyldithiocarbamate) and catalase (3-amino-1,2,4-triazole and salicylic acid) were also examined.
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