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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
Dimercaprol chemical structure | |
2,3-disulfanylpropan-1-ol IUPAC name | |
CAS number 59-52-9 |
ATC code V03AB09 |
PubChem 3080 |
DrugBank [1] |
Chemical formula | {{{chemical_formula}}} |
Molecular weight | 124.227 |
Bioavailability | {{{bioavailability}}} |
Metabolism | {{{metabolism}}} |
Elimination half-life | {{{elimination_half-life}}} |
Excretion | {{{excretion}}} |
Pregnancy category | {{{pregnancy_category}}} |
Legal status | {{{legal_status}}} |
Routes of administration | {{{routes_of_administration}}} |
Dimercaprol (INN) or British anti-Lewisite (abbreviated BAL), is a compound developed by British biochemists at Oxford University during World War II.[How to reference and link to summary or text] It was developed secretly as an antidote for Lewisite, the now-obsolete arsenic-based chemical warfare agent.[How to reference and link to summary or text] Today, it is used medically in treatment of arsenic, mercury and lead, and other toxic metal poisoning.[How to reference and link to summary or text] In addition, it has in the past been used for the treatment of Wilson's disease, a genetic disorder in which the body tends to retain copper.[1]
Biochemical function[]
Heavy metals act by chemically reacting with adjacent sulfhydryl residues on metabolic enzymes, creating a chelate complex that inhibits the affected enzyme's activity.[How to reference and link to summary or text] Dimercaprol competes with the sulfhydryl groups for binding the metal ion, which is then excreted in the urine.[How to reference and link to summary or text]
Dimercaprol is itself toxic, with a narrow therapeutic range and a tendency to concentrate arsenic in some organs. Other drawbacks include the need to administer it by painful intramuscular injection.[How to reference and link to summary or text] Serious side effects include nephrotoxicity and hypertension.
BAL has been found to form stable chelates in vivo with many toxic metals including inorganic mercury, antimony, bismuth, cadmium, chromium, cobalt, gold, and nickel. However, it is not necessarily the treatment of choice for toxicity to these metals. BAL has been used as an adjunct in the treatment of the acute encephalopathy of lead toxicity. It is a potentially toxic drug, and its use may be accompanied by multiple side effects. Although treatment with BAL will increase the excretion of cadmium, there is a concomitant increase in renal cadmium concentration, so that its use in case of cadmium toxicity is to be avoided. It does, however, remove inorganic mercury from the kidneys; but is not useful in the treatment of alkylmercury or phenyl mercury toxicity. BAL also enhances the toxicity of selenium and tellurium, so it is not to be used to remove these metals from the body.[How to reference and link to summary or text]
See also[]
References[]
- ↑ Denny-Brown D, PORTER H (December 1951). The effect of BAL (2,3-dimercaptopropanol) on hepatolenticular degeneration (Wilson's disease). N. Engl. J. Med. 245 (24): 917–25.
- British anti-Lewisite Molecule of the Month, University of Bristol School of Chemistry
- Casarett and Doull's Toxicology, the basic science of poisons [Incomplete reference?]
Template:Antidotes Template:Chelating agents
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