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British antilewisite

Bristol-type machine Bristuron Britannia metal British antilewisite... [Pg.129]

British antilewisite (BAL[2,3-dimercaptopropanol]), dimercaprol DMPS (2,3-dimercapto-l-propanesulfonic acid)... [Pg.54]

The distribution of chromium in human body tissue after acute oral exposure was determined in the case of a 14-year-old boy who ingested 7.5 mg chromium(VI)/kg as potassium dichromate. Despite extensive treatment by dialysis and the use of the chelating agent British antilewisite, the boy died eight days after admission to the hospital. Upon autopsy, the chromium concentrations were as follows liver,... [Pg.163]

BAL = British antilewisite DMPS = 2,3-dimercapto-1-propane sulfonic acid, sodium salt 15S5 = 1,4,7,10,13-pentathiacyclopentadecane 9S3 = 1,4,7-dithiacyclononane. [Pg.2583]

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... [Pg.121]

The pharmacological tools to detoxify arsenicals are sulphydryl reagents. The classic drug for that purpose is 2,3-dimercapto-l-propanol, dimercaprol (British antilewisite, BAL). Since this compound has side effects and a low safety ratio, new analogs with less adverse effects have been developed, e.g. dimercaptopropanesulphonate, dimercaptosuc-cinic acid and dithioerythritol . The efficiency and toxicity of these agents need to be further evaluated. [Pg.720]

The oil-soluble BAL (British antilewisite 2,3-dime-rcaptopropanol) administered intramuscularly appears... [Pg.151]

Treatment follows decontamination of the patient, after donning protective gear. The various agents may vary in their ability to generate local and systemic pathology however, the general treatment principles remain the same for all vesicants except for the availability of British Antilewisite (BAL) for dichloroarsine exposure. [Pg.321]

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. [Pg.667]

BAL (British Antilewisite), Pages 206-207, Sharmilee P. Sawant and Harihara M. Mehendale SummaryPlus Full Text + Links PDF (58 K)... [Pg.800]

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. [Pg.1518]

British antilewisite (BAL) or dimercaprol was developed as an antidote for lewisite. It is used in medicine as a chelating agent for heavy metals. Although BAL can cause toxicity itself, evidence suggests that BAL in oil administered intramuscularly will reduce the systemic effects of lewisite. BAL skin and ophthalmic ointment decrease the severity of skin and eye lesions when applied immediately after early decontamination, but neither of these ointments is currently manufactured. [Pg.1524]

Normally British Antilewisite (2,3-dimercaptopropa-nol BAL), administered intramuscularly, is used as an antidote for mercury poisoning. Oral D-penicilla-mine has been used for less severe cases. The Tacetyl derivative has been tested with good results. Experimentally, oral m-2,3-dimercaptosuccinic acid and the less toxic 2,3-dimercaptopropane-l-sulfonate are more effective than BAL. [Pg.1623]

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. [Pg.1684]

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. [Pg.2359]

Clinical management is supportive and there no known active treatment. Administration of table salt will help precipitate soluble silver as the insoluble silver chloride. British antilewisite (2,3-dimercapto-propanol) has not proven useful. [Pg.2409]

Vitamin C (ascorbic acid) reduces the characteristic garlic breath however, it may also adversely affect the kidneys when an excess amount of tellurium is present. BAL (British antilewisite 2,3-dimer-captopropanol) is contraindicated since it enhances the toxicity of tellurium. There are no available treatments for poisoning. [Pg.2533]

For acute exposure, ipecac should be administered and lavage performed. The use of single- or multiple-dose activated charcoal is supported by in vitro binding experiments and some animal data, and charcoal hemoperfusion may be a useful adjunct. Forced potassium diuresis appears to be harmful. Flemodial-ysis is also recommended with potassium administration. Since calcium metabolism is disturbed, supplementary calcium is indicated. The use of traditional metal chelators such as dimercaprol (British antilewisite) and penicillamine is not supported by the available evidence. In fact, the use of penicillamine may lead to redistribution of thallium into the central nervous system. Multiple animal studies have found evidence of enhanced elimination and improved survival with Prussian blue however, despite the fact that many humans have been treated with Prussian blue, the data presented are insufficient to judge its true efficacy. Despite this, one publication notes that... [Pg.2557]

See also Animals, Poisonous and Venomous BAL (British Antilewisite) Food and Drug Administration, US Toxicology. [Pg.2761]

Clinical management is supportive. Chelating agents such as British Antilewisite (2,3-dimercaptopro-panol) or o-penicillamine are not effective. [Pg.2871]

Clinical management is supportive. Gastric decontamination should be considered only in the case of massive ingestions. Normal zinc levels in the blood are between 68 and 136pgdl . Chelating agents such as BAL (British Antilewisite 2,3-dimercapto-propanol) or calcium EDTA will enhance removal of zinc, but are not likely indicated unless the unusual case of massive chronic exposure. Hemodialysis and other methods of extracorporeal elimination are not necessary. [Pg.2873]

In comparison to the majority of odier heavy metals, tungsten and most of its compounds possess very low toxicity, if at all. Intoxications occur rarely, almost exclusively by occupational exposure. As treatment in acute poisoning, Dimercaprol (British Antilewisite) may be useful. [Pg.413]

Stocken LA and Thompson RHS (1946). British antilewisite, arsenic and thiol excretion in animals after treatment of lewisite burns. Biochem J, 40, 548-554. [Pg.475]

Vilensky JA and Redman K (2003). British antilewisite (dimercaprol) an amazing history. Ann... [Pg.475]

BAL, British antilewisite dimercaprol, 2,3-dimercaptopropanol (antidote for poisoning caused by heavy metals forms very stable metal complexes)... [Pg.1678]

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). [Pg.1127]

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. [Pg.511]


See other pages where British antilewisite is mentioned: [Pg.381]    [Pg.276]    [Pg.267]    [Pg.273]    [Pg.998]    [Pg.381]    [Pg.129]    [Pg.54]    [Pg.2587]    [Pg.1548]    [Pg.377]    [Pg.2997]    [Pg.267]    [Pg.1376]    [Pg.927]    [Pg.2586]   
See also in sourсe #XX -- [ Pg.1376 ]




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