Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred thirty children aged 1 to 8 years with blood lead levels greater than 50 micrograms/100 ml of whole blood (WB) and free erythrocyte protoporphyrin (FEP) concentration greater than 250 micrograms/100 ml of WB received 207 chelation treatments for plumbism. All chelation treatments consisted of CaNa2 ethylenediaminetetraacetic acid (EDTA) 25 mg/kg per dose every 12 hours and 2,3-dimercapto-1-propanol (BAL) 3 mg/kg per dose every four hours for five days. Seventeen children demonstrated transient doubling of pre-chelation treatment serum creatinine (less than or equal to 2.0 mg/100 ml) during or following chelation treatment; 5/17 also had mild proteinuria. Four children developed severe oliguric (greater than 250 ml/sq m/day) acute renal failure. Serum creatinine levels were elevated six to seven days after chelation treatment was started and reached maximal values of 3.9 to 8.4 mg/100 ml, three to six days later. Renal function returned to pre-chelation treatment values during the subsequent six to 18 days. In the 21 nephrotoxic patients and the 109 nontoxic patients there were no significant differences in age (3.8 +/- 0.6 vs 3.2 +/- 0.2 years), sex (61% vs 53% males), percent who received multiple chelation treatments (38% vs 30%), blood lead levels (85 +/- 5 vs 79 +/- 1 microgram/100 ml of WB), FEP (380 +/- 30 vs 382 +/- 18 micrograms/100 ml of WB), hemoglobin (11.5 +/- 0.4 vs 11.1 +/- 0.2 gm/100 ml, and pre-chelation treatment serum creatinine (0.46 +/- 0.06 vs 0.58 +/- 0.03 mg/100 ml). It was concluded that 13% of children with plumbism who received chelation treatments developed mild transient biochemical evidence of nephrotoxicity and another 3% developed acute renal failure characterized by oliguria four to eight days after chelation treatment was discontinued.
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PMID:Reversible nephrotoxic reactions to a combined 2,3-dimercapto-1-propanol and calcium disodium ethylenediaminetetraacetic acid regimen in asymptomatic children with elevated blood lead levels. 709 93

The distribution and excretion of mercury were studied in mice and rats given a single injection of HgCl2 combined with chelation treatment. BAL-sulph (2,3-dimercaptopropane-1-sulphonate) given intravenously (500 mumol SH/kg) to mice 24 hrs after the mercury injection (2.0 mumol Hg/kg) reduced the kidney Hg-level significantly, while NAPA (N-acetyl-DL-penicillamine) and BAL (2,3-dimercaptopropanol) did not. Severe kidney damage with oliguria was observed in pregnant as well as in non-pregnant rats after injection of 5 mumol/kg of HgCl2. The gross pathological changes could be avoided with immediate treatment with BAL-sulph (500 mumol SH/kg), and such treatment protect against the oliguric reaction. Treatment delayed for 24 hrs reduced the renal Hg-levels significantly, but was ineffective in preventing the kidney damage. This indicates that irreversible changes might have occurred in kidneys cells at this time. The Hg-levels in the brain were either unchanged or lowered in animals given BAL-sulph treatment. BAL-sulph is supposed to act by chelation Hg++, particularly in the extracellular space. The complexes formed appears to be rapidly excreted by healthy kidneys. Mercury poisoning with severe renal damage is, however, associated with a block in urinary Hg-excretion. The poisoned animals responded on the BAL-sulph treatment with a substantial raise of faecal mercury excretion.
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PMID:The effect of immediate and delayed treatment with 2,3-dimercaptopropane-1-sulphonate on the distribution and toxicity of inorganic mercury in mice and in foetal and adult rats. 736 70