Mechanism of action
Arsenic and some other heavy metals act by chelating with adjacent thiol residues on metabolic enzymes, creating a chelate complex that inhibits the affected enzymes activity. Dimercaprol competes with the thiol groups for binding the metal ion, which is then excreted in the urine.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. Serious side effects include nephrotoxicity and hypertension. Dimercaprol has been found to form stable chelates in vivo with many other 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. Dimercaprol 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 dimercaprol 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 phenylmercury toxicity. Dimercaprol also enhances the toxicity of selenium and tellurium, so it is not to be used to remove these elements from the body.
History
The original name of dimercaprol reflects its origins as a compound secretly developed by British biochemists at Oxford University during World War II as an antidote for lewisite, a now-obsolete arsenic-based chemical warfare agent. See also
EDTA
2,3-Dimercapto-1-propanesulfonic acid
Dimercaptosuccinic acid
DMSA scan
Penicillamine
Heavy metal poisoning

References
External links
"Dimercaprol". Drug Information Portal. U.S. National Library of Medicine.