Disulfiram and its Metabolite, Diethyldithiocarbamate: by Peter K. Gessner, Teresa Gessner (auth.)

By Peter K. Gessner, Teresa Gessner (auth.)

This ebook is aimed toward these within the biomedical group which are drawn to the healing purposes, pharmacology, biochemistry, toxicology and pharmacokinetics of the name compounds. contemporary findings in regards to the skill of diethyldithiocarbamate (ditiocarb, Imuthiol®) to hold up the development of HN infections and AIDS, the invention of its capability as a rescue agent in melanoma chemotherapy, and the identity of disulfiram (Antabuse®) regimens that let alcoholics to accomplish abstinence of many months' period have made scripting this ebook a thrilling adventure. whilst the truth that the 2 medications range considerably of their pharmacological results regardless of their effortless interconvertibility has rendered the writing intellec­ tually hard. Diethyldithiocarbamate, an agent possible much less poisonous than aspirin, opponents it within the multiplicity and variety of its pharmacological right­ ties. striking between those are the manyfold powerful immunostimulant results, and notwithstanding every one of these contain results on T -cells, the mechanism of diethyldithiocarbamate's motion is still faraway from transparent. The drug can be a powerful chelator of heavy metals and this has ended in a few medical functions. As may be anticipated, it inhibits numerous very important enzymes. extra, it really is some of the most powerful radioprotective brokers; it additionally protects organisms opposed to quite a few poisonous agents.

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Extra resources for Disulfiram and its Metabolite, Diethyldithiocarbamate: Pharmacology and status in the treatment of alcoholism, HIV infections, AIDS and heavy metal toxicity

Sample text

76 mM DmSMe Oohansson, 1989c). 6 ~M DmSMe causes a 75% inhibition of the low-I<:;" ALDH. 9). Taken together the above observations strongly suggest that the ultimate. highly potent, inhibitor of the low-Km ALDH is a further metabolite of DmSMe, rather than DmSMe itself. Such a metabolite may be generated by the enzyme(s) present in tissue homogenates, or in intact cells, when such preparations are used in the assays with either DmSMe or DSMe.

9). Using the same method, Johansson and Stankiewicz (1985) reported that upon addition of 5 nmol DSSD per ml of blood or plasma, all of it is reduced with the formation of Cu(DS)z. Addition of the alkylating mixture of mercaptoethanol and ethyl iodide to plasma aliquots results in all of the DS moiety being ethylated to DSEt. Johansson (1986) reported recoveries from plasma of 95% and 100% for DSMe and DSH, respectively. Because DSSD cannot be recovered from plasma when the latter is injected onto the precolumn without additions Oohansson, 1986), an alternative procedure was devised.

3 FORMATION OF MIXED DISULFIDES . . . . . . 4 UPTAKE OF DISULFIRAM BY BLOOD CELLS . . . 5 SUMMARY . . . . . . . . . . . . . . . . . . 1 INTRODUCTION Disulfiram (DSSD) and diethyldithiocarbamate (DSH) interact with blood constituents in a variety of ways which are still poorly understood. Nevertheless these interactions are central to the design and evaluation of analytical procedures, as well as to the interpretation of experimental results and their biological consequences.

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