Dimercaptopropanol Antilewisite

British antilewisite (BAL[2,3-dimercaptopropanol]), dimercaprol DMPS (2,3-dimercapto-l-propanesulfonic acid)... 

SYNS BRITISH ANTILEWISITE DICAPTOL DIMERCAPROL PROPANOL DIMERCAPTOL 2,3-DIMERCAPTOL-l-PROPANOL DIMERCAPTOPRO-PANOL 2,3-DIMERCAPTOPROPANOL 2,3-DIMERCAPTOPROPAN-l-OL DITHIOGLYCEROL 1,2-DITHIOGLYCEROL 2,3-DITHIOPROPANOL SULFACTIN USAF ME-1... 

For acute toxicity, emesis is recommended. Treatment is symptomatic. A combination of BAL (British AntiLewisite 2,3-dimercaptopropanol) and calcium-ethylene diamine tetraacetic acid has been used successfully in a poisoned infant. Penicillamine has also been used. Recently, oral administration of 2,3-dime-rcaptol-propane sulfonate was found to be effective in experimental rodents. Electrolyte balance must be maintained when gastric lavage is indicated. Potassium ferrocyanide should be added to precipitate the copper. 

Chelation therapy is usually the treatment of choice. Both CaNai-EDTA (calcium disodium salt of ethylenediaminetetraacetic acid) and British Antilewisite compound (BAL 2,3-dimercaptopropanol) are commonly used to remove lead from the body. Both are administered via intramuscular injection. BAL binds lead to sulfhydral groups and chelates metal from both inside and outside the cellular space. Lead removal through the bile and urine is increased within 30 min of administration. BAL is the common choice when there is known toxicity to the kidney, but it is contraindicated if there is liver failure or glucose-6-phosphate dehydrogenase deficiency. BAL treatment has produced a number of adverse reactions, including nausea, vomiting, tachycardia, and fever. 

There is no known useful treatment for methylmercury poisoning. A variety of chelating agents, such as D-penicillamine, l-acetyl-D,L-penicillamine, thiol resins, activated charcoal, BAL (British Antilewisite 2,3-dimercaptopropanol), and meso-2,3-dime-rcaptosuccinic acid, have been used to treat methyl-mercury exposure but with limited to no success. 

Currently, there are no antidotes of choice for selenium toxicity. Ethylenediaminetetraacetic acid and BAL (British antilewisite 2,3-dimercaptopropanol) should not be used because they may enhance selenium toxicity. Treatment is symptomatic (e.g., cardiopulmonary). Often, supplemental oxygen is needed. Corrosive selenious acid (in gun-bluing solution) should be treated similar to other agents that cause esophageal burns. 

BAL, British antilewisite dimercaprol, 2,3-dimercaptopropanol (antidote for poisoning caused by heavy metals forms very stable metal complexes)... 

Dimercaprol (2,3-dimercaptopropanol) was developed during World War 11 as an antidote to lewisite, a vesicant arsenical war gas, hence its alternative name, British antilewisite (BAL). 

A. Dimercaprol Dimercaprol (2,3-dimercaptopropanol BAL [British antilewisite]) is a biden-tate chelator, ie, it forms two bonds with the metal ion, preventing the metal s binding to tissue proteins and permitting its rapid excretion. 

Synonyms BAL British antilewisite Dicaptol Dimercaprol Dimercaprol propanol Dimercaptol 2,3-Dimercaptol-1-propanol 2,3-Dimercaptopropanol 2,3-Dimercaptopropan-1-ol Dithioglycerol... 

BAL or British antilewisite (= 2,3-dimercaptopropanol) must be considered to be the first antidote conceived from logical, biochemical reasoning. If administered after lewisite has been in contact with the skin or conjunctiva, but before irreversible anatomical lesions are established, the oedema and inflammation regress and no cell destruction occurs. The BAL story must be considered as being the most important event which established the reputation of biochemical pharmacology as a useful concept... 

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