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)

In massive arsenic poisoning, the use of hemodialysis and dimercaprol (BAL) therapy is still controversial. Hemodialysis is thought of value only for supportive care. BAL therapy has been criticized because of its delayed action, its own toxicity and its possible influence on arsenic clearance during hemodialysis. We studied arsenic kinetics during an acute suicidal intoxication (10 g of sodium arsenate). Treatment included gastric lavage, oral charcoal and supportive measures. Hemodialysis was performed immediately and repeated the next day. BAL therapy was prescribed only on the second day. Cardiovascular collapse, anuria and hepatic disturbance recovered in a few days and the patient could be discharged on the 15th day. Instantaneous serum arsenic hemodialysis clearance was 85 +/- 75 ml/min without previous BAL injection and 87.5 +/- 75 ml/min with a previous 250 mg BAL injection (difference not significant) indicating that BAL did not impede arsenic dialysis. The calculated total hemodialysis clearance of arsenic was higher than mean serum hemodialysis clearance indicating that erythrocyte bound arsenic is also eliminated during dialysis. We propose to consider early hemodialysis as an elimination measure in massive arsenic poisoning and to choose BAL as a chelator when dialysis is required.
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PMID:Massive arsenic poisoning--effect of hemodialysis and dimercaprol on arsenic kinetics. 157 49

The effects of some new chelating agents on the cadmium burden of CHO cells in culture were investigated. The chelators were sodium-N-(4-methoxybenzyl)-D-glucamine-dithiocarbamate (MeOBG-DTC), sodium-N-benzyl-D-glucaminedithiocarbamate (BG-DTC) and diisopropylmeso-2,3-dimercapto succinate (DiP-DMSA). The results were compared with the effect of the well known dimercaptopropanol (BAL). The derivates of dithiocarbamate are much less toxic than DiP-DMSA and BAL. All chelators effectively prevent Cd uptake into the cells. Mobilization of intracellular Cd, however, is more effective by the DTC-derivatives than by DiP-DMSA or BAL. Within the cell the major fraction of Cd after 48 hours incubation is found in the nuclei and cytosol and very little in the peroxisomes. The chelating agents remove the metal mostly from nuclei and cytosol. Incubation of the cells with cadmium leads to the induction of a Cd binding protein of an apparent molecular weight of 12500 Da, presumably metallothionein. MeOBG-DTC is more effective in removing the metal from this protein than BG-DTC.
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PMID:Effects of chelating agents on the cadmium burden of cells in culture. 165 37

1. Arsenite and arsenate poisoned rats were treated with either BAL (2,3-dimercapto-1-propanol), penicillamine (PA) (beta-beta dimethyl cystein) or selenium (Se) (as sodium selenite). 2. The minimal dose of each antagonist that treated arsenic-induced lethality (causing 100% survival) was the same for both arsenite and arsenate. 3. Arsenic mobilization from the tissues (blood, kidney, liver, lungs, spleen, muscles, brain, heart) and its excretion in urine and feces were higher in arsenite-intoxicated animals than in arsenate-intoxicated ones. 4. The effect of each antagonist, when injected alone, on the urinary and fecal excretion of endogenous metals (Cu, Zn, Fe, Ca and Mg) was also examined. 5. The results indicated marked differences in the relative ability of BAL, PA and Se to increase the excretion of the metals.
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PMID:Effect of some arsenic antagonists on the toxicity, distribution and excretion of arsenite and arsenate in rats. 168 7

The effect of two vicinal dithiols, 2,3-dimercaptopropan-1-ol (BAL) and N-(2,3-dimercaptopropyl)phthalamidic acid (DMPA), and a dithiocarbamate, sodium N-(4-methoxybenzyl)-D-glucamine dithiocarbamate (MeOBGDTC), on the biliary excretion of cadmium was examined in rats. Tissue cadmium levels were also determined following the measurements of biliary excretion of cadmium. At 30 min after the injection of CdCl2.2.5H2O (1 mg/kg, iv) each rat was given 400 mumol/kg ip of one of the compounds, BAL, DMPA or MeOBGDTC. While all the compounds increased the biliary excretion of cadmium, the most effective was MeOBGDTC, whose administration resulted in a 580% increase in biliary cadmium content. The effectiveness of the MeOBGDTC may be due to the presence of both nonpolar and nonionizing polar groups attached to nitrogen. MeOBGDTC was able to mobilize cadmium to the bile even after the occurrence of the synthesis of metallothionein and the incorporation of the cadmium into it. An attempt was also made to determine the chemical nature of the Cd-MeOBGDTC complex present in the bile by comparing a newly synthesized authentic sample of Cd(MeOBGDTC)2 complex with the hot dioxane extract of the freeze-dried bile samples using thin-layer chromatography and proton NMR. The results suggested that cadmium excreted in the bile in part, is complexed to MeOBGDTC and glutathione.
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PMID:A comparative study of the influence of vicinal dithiols and a dithiocarbamate on the biliary excretion of cadmium in rat. 189 71

The consequences of the mobilization of aged intracellular cadmium from its in vivo deposits in mice by chelating agents were examined. The chelating agents used were BAL, sodium N-benzyl-D-glucamine dithiocarbamate (NaB), Diisopropyl meso-2,3-dimercaptosuccinate(Di-PDMS) and sodium N-(4-methoxybenzyl)-D-glucamine dithiocarbamate(4-Me0), all previously shown capable of causing statistically significant decreases in either renal or hepatic cadmium burdens in rodents. They were given at a level of 400 mumol/kg (i.p.) daily for 10 days to mice previously loaded with a total of 10 mg CdCl2.2.5 H2O/kg. Under these conditions a significant decrease in the renal cadmium level occurred following treatment with BAL, NaB, and 4-MeO; hepatic cadmium levels decreased significantly following treatment with NaB and 4-MeO. Pathological examination of the kidneys, liver, and testes in these animals showed that chelate mobilization of the cadmium produced no noticeable changes in the histopathology of these organs in comparison with that observed for the animals which had been given only cadmium and had undergone no chelate treatment. The results suggest that the mobilization of such aged cadmium from in vivo deposits need not result in any deleterious changes in the kidneys, liver or testes.
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PMID:Intracellular cadmium mobilization sequelae. 231 52

The efficacy of several chelating agents in alleviating acute lead intoxication has been investigated in male Swiss mice. The relative effectiveness of diethylenetriaminepentaacetic acid (DTPA), ethyleneglycolbis-(beta-amino-ethylether)-N,N'-tetraacetic acid (EGTA), cyclohexanediaminetetraacetic acid (CDTA), L-cysteine, N-acetyl-L-cysteine (NAC), ascorbic acid, sodium diethyldithiocarbamate (DDC), 2,3-dimercaptosuccinic acid (DMSA) and sodium 2,3-dimercapto-1-propanesulfonate (DMPS) in reducing lethality of lead was examined. Significant increases in survival were noted with CDTA, ascorbic acid, DMSA, and DMPS. Therapeutic effectiveness (TEF) was determined for these compounds; TEF for ethylenediaminetetraacetic acid (EDTA) and for 2,3-dimercaptopropanol (BAL) was also determined; CDTA (2.33) and EDTA (1.73) showed the highest values. In subsequent experiments, the effect of the chelating agents on the distribution and excretion of lead was investigated. Lead acetate trihydrate was administered subcutaneously at doses of 37.8 mmol/kg (LD50), and fifteen minutes later, chelators were given intraperitoneally at doses approximately equal to one-fourth of their respective LD50 values. EDTA, DTPA and CDTA were the most effective agents in increasing the urinary excretion of lead, whereas DTPA, CDTA, and DDC increased significantly the fecal excretion of lead. EDTA, DDC, and CDTA were the most effective chelators in reducing the concentration of lead found in various tissues. On the basis of these results, CDTA may be considered as an alternative in the treatment of acute lead poisoning.
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PMID:Treatment of acute lead intoxication. A quantitative comparison of a number of chelating agents. 232 19

A 29-year-old man was found unresponsive a few minutes after self-injecting undetermined amounts of potassium cyanide and sodium arsenite intravenously in a suicide attempt. Treatment with the Lilly Cyanide Antidote kit rapidly resolved the initial coma, despite a whole blood cyanide level of 4.4 micrograms/mL. A 12-hour urine arsenic collection begun on admission showed 10,065 micrograms arsenic/12 hr. The patient received intramuscular BAL initially, which was followed by two ten-day courses of oral D-penicillamine. Complications included upper gastrointestinal tract bleeding requiring transfusion, transient elevations of liver function tests, self-limited complaints of decreased vision with conjunctival hyperemia and photophobia, and an abscess at the injection site. Although specific antidote therapy completely resolved the cyanide toxicity, early and prolonged arsenic chelation did not prevent a mild sensory peripheral neuropathy from developing with onset about 17 days after self-injection.
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PMID:Cyanide and arsenic poisoning by intravenous injection. 253 98

A genomic library of Streptococcus pyogenes CS24 DNA was constructed by cloning streptococcal DNA partially digested with Sau3A into the lambda replacement vector EMBL3. The expression of streptococcal C5a peptidase (SCP) was analyzed by radioimmunoassay with hyperimmune rabbit serum. Two clones, lambda 4.1 and lambda 4.2, were found to express the desired antigen, and various DNA fragments from the hybrid bacteriophage lambda 4.1 were subcloned into the plasmid vector pUC9 in Escherichia coli. One of the recombinant plasmids, designated pTT1, contained a 5.8-kilobase (kb) streptococcal DNA insert. Analysis of total cellular protein from this E. coli clone by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western (immuno-) blotting identified a 140,000-Mr protein, similar in size to the native protein purified from S. pyogenes. Cloned SCP was functionally active, as shown by its ability to inhibit C5a-mediated chemotaxis. By deletion analysis with both restriction endonucleases and BAL 31 nuclease, the SCP gene was localized to a 4.3-kb segment of DNA. Southern hybridization experiments showed that the type 12 M protein-coding sequence is also present in the hybrid phage lambda 4.1, at approximately 2 kb upstream of the SCP structural gene. Western blot analysis indicated that the cloned streptococcal DNA in lambda 4.1 directed the expression of both SCP and M12 protein.
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PMID:Cloning and expression of the streptococcal C5a peptidase gene in Escherichia coli: linkage to the type 12 M protein gene. 254 63

A three-year-old child died after ingestion of a mouthful of an estimated 44% sodium arsenite solution. Litigation was initiated based on the quality of emergency treatment at a rural hospital. An issue raised in litigation was whether the child could have survived if he had received an additional dose of BAL (dimercaprol). BAL had been sent for from a neighboring city and arrived approximately 2.0 h after admission. The first 50-mg dose of BAL could have combined with a maximum of 30 mg arsenic; a second dose could have brought the total of chelated arsenic to 60 mg. To determine the total body burden of arsenic in the child, multiple tissues were analyzed. The total body burden was estimated at 113 mg, with 100 mg of this total attributable to the ingested solution. The actual body burden after two doses of BAL therefore would have been at least 40 mg, a fatal level.
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PMID:Estimation of the body burden of arsenic in a child fatally poisoned by arsenite weedkiller. 261 44

The effects of three chelating agents, sodium N-benzyl-D-glucamine dithiocarbamate(NBG-DTC), 2,3-dimercaptopropanol(BAL), and D-penicillamine(D-PEN), on the distribution, excretion, and renal toxicity of inorganic mercury were compared in rats exposed to HgCl2. Rats were injected i.p. with 203HgCl2 (300 micrograms of Hg and 2 microCi of 203Hg/kg) and 30 min or 24 h later they were injected with a chelating agent (a quarter of an LD50). The injection of the chelating agents significantly enhanced the biliary and urinary excretions of mercury. BAL was the most effective for removal of mercury from the body at 30 min after mercury treatment. The extent of enhancing effect of the chelating agents for removal of mercury at 24 h after mercury was in the order NBG-DTC = BAL greater than D-PEN. The injection of BAL at 24 h after mercury treatment caused the redistribution of mercury to the heart and lung. NBG-DTC did not result in the redistribution of mercury to the heart, lung, and brain. Urinary excretion of protein and AST significantly increased 24-48 h after mercury treatment and decreased to the control values 72 h after mercury. The injection of the chelating agents at 30 min after mercury treatment significantly decreased the urinary excretion of protein and AST. In rats pretreated with mercury 24 h earlier, the chelating agents significantly decreased the urinary protein at 48 h after mercury treatment, but did not decrease the urinary AST. The results of this study indicate that the chelating agents are effective in removing mercury from the body, resulting in the protective effect against the mercury-induced renal damage.
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PMID:Comparative effects of chelating agents on distribution, excretion, and renal toxicity of inorganic mercury in rats. 278 Nov 44


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