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)

The optimal reaction conditions and kinetic properties of eleven leukocyte acid hydrolases determined with the use of fluorigenic derivatives of 4-methyl-umbelliferone are described. The enzymes studied were acid phosphatase, aryl sulfatase, alpha- and beta-glucosidase, alpha- and beta-galactosidase, alpha-mannosidase, N-acetyl-beta-glucosaminidase, N-acetyl-beta-galactosaminidase, beta-glucuronidase and alpha-fucosidase. More than 90% of the activity of each enzyme was released into a 27,000 X g supernatant by a double sonication procedure employing 0.9% sodium chloride and 0.1% Triton X-100. The Km values obtained were similar to those previously reported for chromogenic subtrates. A single Km value could not be derived for beta-galactosidase because its double reciprocal plot was not linear. All enzymes could be measured with less than 10 mug of protein within 15 min. Activators and inhibitors studied included the chloride salts of Na+, K+, Zn2+, Ca2+, Mg2+, Hg2+, and Fe2+ as well as p-chloromercuriphenysulfonate, glutathione, BAL, EDTA, EGTA, Triton X-100 and sodium taurocholate. The reaction conditions described in this report can be used for the diagnosis of various lysosomal storage diseases and should facilitate the development of automated procedures for the analysis of these eleven enzyme activities with small quantities of blood.
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PMID:Human leukocyte acid hydrolases: characterization of eleven lysosomal enzymes and study of reaction conditions for their automated analysis. 0 26

Arsenic (As2O3)-poisoned rats were treated with either 2,3-dimercaptosuccinic acid (DMS) or dimercaptopropanol (BAL) at doses of 30 mg/kg/day. A control group received no treatment. The total quantity of arsenic excreted was not significantly different in response to 4 days of treatment with either DMS or BAL. In addition, there was no difference between the two drug treatment groups in the residual arsenic content of brain, liver, kidney and spleen after treatment. Both drugs reduced the arsenic content of each tissue to approximately 40% of that of untreated controls. Previous studies have shown that DMS is orally effective for the treatment of lead poisoning. The LD50 of DMS was determined to be in excess of 3 g/kg in rats and mice, approximately 30 times the LD50 of BAL. No gross, histopathological or biochemical evidence of toxicity was observed in mice, rats or dogs which received DMS 5 days per week for 6 months. DMS did not affect the excretion of zinc, iron, calcium or magnesium. Urinary copper excretion was significantly elevated in response to 30 mg/kg of DMS, suggesting that the drug might also be useful for the treatment of Wilson's disease.
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PMID:The pharmacology of 2,3-dimercaptosuccinic acid and its potential use in arsenic poisoning. 21 41

A smelter exposed to zinc fumes reported severe recurrent episodes of cough, dyspnea and fever. Bronchoalveolar lavage showed a marked increase in lymphocytes count with predominance of CD8 T-lymphocytes. Presence of zinc in alveolar macrophages was assessed by analytic transmission electron microscopy. This is the first case of recurrent bronchoalveolitis related to zinc exposure in which the clinical picture and BAL results indicate a probable hypersensitivity pneumonitis.
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PMID:Occupational hypersensitivity pneumonitis in a smelter exposed to zinc fumes. 154 Nov 64

The effectiveness of CaEDTA alone vs CaEDTA plus BAL was compared retrospectively in a group of 72 children with lead levels between 2.41 mumol/L (50 micrograms/dL) and 2.90 mumol/L (60 micrograms/dL). The children who received both drugs had higher median zinc protoporphyrin (ZnP) concentrations at the initiation of therapy than children who received CaEDTA alone (160 micrograms/dL vs 96 micrograms/dL, p less than .01). There was a significantly increased incidence of vomiting and abnormal liver-function test results in the children who received both drugs. The children who received CaEDTA alone had a greater percent mean fall in lead level at one to three weeks postchelation (30.5% vs 18.1%, p less than .05). Children who received both CaEDTA and BAL had a greater percent decrease in ZnP at four to eight months postchelation, but there was no difference in percent decrease in lead levels. Children who received both drugs also had a greater number of repeat courses of chelation by six months. The addition of BAL to CaEDTA for treatment of children with lead levels of 2.41 mumol/L (50 micrograms/dL) to 2.90 mumol/L (60 micrograms/dL) produced greater toxicity and does not seem to prevent repeat chelations within six months.
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PMID:CaEDTA vs CaEDTA plus BAL to treat children with elevated blood lead levels. 161 61

The relative abilities of approximately 20 chelating agents to act as antagonists for acute and chronic lead poisoning have been examined in the mouse. The acute LD50 for lead acetate trihydrate was determined and found to be 135.3 mg Pb/kg for i.p. injection with a 95% confidence interval of 87.1-210.3 mg Pb/kg. The relative efficacy of chelating agents to reduce liver, kidney, spleen, bone and brain levels of lead was determined. The movement of lead from the liver to the bone was followed during the first 7 days post injection and was found to result in appreciable changes in the lead levels of these organs from day to day during this entire period. Of the compounds examined, the ones which were most effective in mobilizing lead under various conditions included meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropane-1-sulfonate (DPMS), disodium calcium ethylene-diaminetetraacetate (Na2CaEDTA), trisodium zinc triethylenetetraminehexa-acetate, dicalcium ethylenediaminetetra(methylenephosphonate) (Ca2EDTPO) and diethyl dimercaptosuccinate (DEMSA) and 2,3-dimercapto-1-propanol (BAL).
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PMID:Comparative mobilization of lead by chelating agents. 321 88

Diabetogenic action of dithisone was investigated in a total of 368 adult rabbits and 53 young animals between 10 h and 31 days of age. The diabetes was found in 95% of animals injected with dithisone and various forms of this disease were observed: 1. long-term diabetes without any signs of normalization of glycemia; 2. diabetes with periodical remissions; 3. several cases with a definite remission. The diabetes did not appear in young animals during certain periods of life in which the concentration of zinc in pancreatic islets was very low. It was possible to prevent the development of this disease by the administration of some compounds containing sulfhydryl or imidazole groups (cysteine, SH-glutathione, dimercaptopropanol (BAL), unithiol (sodium 2,3-dimercaptopropansulfonate), (histidine) and the diabetes also did not appear in such animals in which a majority of zinc was removed by glybenclamide. From these observations it was concluded that the development of diabetes after dithisone depends on the formation of dithisone complex with zinc in beta-cells.
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PMID:Dithisone diabetes in rabbits and its prevention by sulfhydryl and imidazole containing compounds. 643 2

Chelation and removal of cadmium from rats which were exposed to cadmium by multiple injections were studied in vivo after injection of two different compounds, 2,3-dimercaptopropanol (BAL) and diethylenetriamine pentaacetic acid (DTPA). Rats were injected i.p. with 1 mg of Cd/kg as 109CdCl2 daily for 4 days and 3 days after the last injection, they were treated with the chelating agents alone or in combination 5 days in a week for 2 weeks. BAL (50 mg/kg) alone or in combination with DTPA (50 mg/kg) was effective in removing cadmium from the body without increasing the level of cadmium in the kidney, the critical organ in cadmium toxicity. After treatment with BAL alone and BAL-DTPA, cadmium was excreted mainly in the feces with marked decrease in hepatic and renal concentrations of both cadmium and metallothionein. Injection of DTPA alone increased the urinary excretion of cadmium without any significant change in tissue cadmium. Although the urinary excretion of zinc was increased after injection of DTPA and also BAL-DTPA, there was no change in the tissue levels of zinc and copper. The results of this study suggest the potential use of BAL or BAL-DTPA combination as a mode of chelation of cadmium from the body under proper experimental conditions in chronic cadmium poisoning. It may be possible to prevent tubular damage in the kidney, the critical organ in cadmium toxicity by this treatment.
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PMID:Chelation of cadmium from metallothionein in vivo and its excretion in rats repeatedly injected with cadmium chloride. 710 71

The effects of changes in sulfur-containing intracellular ligands on biliary excretion of cadmium were studied in rats. Injection of zinc or copper salts 24 h before intravenous injection of 109CdCl2 (1 mg/kg Cd) decreased biliary excretion of Cd. Pretreatment with cysteine (25 mg/kg) had a similar effect. Depletion of intracellular thiol by injection of diethylmaleate had little effect. The effect of chelating agents on the pharmacokinetics of Cd depended on time of administration of the agents after exposure to Cd. When chelating agents were administered 1/2 h after Cd injection (before the synthesis of metallothionein), the thiol-containing agents (2,3-dimercapto-1-propanol (BAL), DL-penicillamine, N-acetylpenicillamine, and dithioerythritol) increased the biliary excretion of Cd, while the carboxyl-containing ones (EDTA and nitrilotriacetate) increased the urinary excretion of Cd. BAL was the most effective chelating agent, but there was also an increase in the renal concentration of Cd. However, when these chelating agents were administered 24 h after Cd injection (after the synthesis of metallothionein), only BAL increased the biliary excretion of Cd. Renal and hepatic Cd concentrations decreased concurrently after BAL treatment.
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PMID:Biliary excretion of cadmium in rat. III. Effects of chelating agents and change in intracellular thiol content on biliary transport and tissue distribution of cadmium. 739 99

A 16-month-old boy ingested liquid zinc chloride/ammonium chloride soldering flux. He developed severe local burns, metabolic acidosis, hepatic damage, hyperamylasemia, lethargy, and hypertension. Peak measured plasma zinc was 1,199 micrograms/dL. Because of persistent signs of systemic toxicity, he was chelated with dimercaprol (BAL) and EDTA. Although clinical improvement was noted coincident with the initiation of chelation, there was no apparent increase in urinary zinc excretion. Scarring in the gastric antrum necessitated an antrectomy. The child recovered without other apparent complications.
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PMID:Acute zinc chloride ingestion in a child: local and systemic effects. 771 Jan 73

Copper is an essential trace element, which is an important catalyst for heme synthesis and iron absorption. Following zinc and iron, copper is the third most abundant trace element in the body. Copper is a noble metal, like silver and gold. Useful industrial properties include high thermal and electrical conductivity, low corrosion, alloying ability, and malleability. Most of the metallic copper appears in electrical applications. Copper is a constituent of intrauterine contraceptive devices and the release of copper is necessary for their contraceptive effects. The average daily intake of copper in the US is about 1 mg Cu with the primary source being the diet. The bioavailability of copper from the diet is about 65-70% depending on a variety of factors including chemical form, interaction with other metals, and dietary components. The biological half-life of copper from the diet is 13-33 days with bilary excretion being the major route of elimination. Copper sulfate is a gastric irritant that produces erosion of the lining of the gastrointestinal tract. Chronic copper toxicity is rare and primarily affects the liver. Wilson's disease and Indian childhood cirrhosis are examples of severe chronic liver disease that results from the genetic predisposition to the hepatic accumulation of copper. The serum copper concentration ranges up to approximately 1.5 mg/L in healthy persons. Gastrointestinal symptoms occur at whole blood concentrations near 3 mg Cu/L. Chelating agents (CaNa2EDTA, BAL) are recommended in severe poisoning, but there are little pharmacokinetic data to evaluate the effectiveness of these agents.
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PMID:Copper. 1038 57


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