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 authors showed that in rat liver and brain sections with blocked SH groups and split S-S bonds mercury orange stains some tissue structures after treating the sections with BAL. Considering that the blockade of SH groups with N-ethylmaleimide in is stable the authors set forth the hypothesis that the use of BAL may enable the demonstration of a sulphur-containing amino-acid which is devoid of SH or SS groups but acquires them only when acted upon by BAL. The in vitro studies demonstrated that the effect of BAL makes it possible to stain methionine with mercury orange which otherwise does not stain this amino-acid.
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PMID:Further studies on the possibility of differential demonstration of radicals of sulphur-containing amino-acids. 5 9

Exposure to mercury vapors for an hour per working day over a period of 13 years produced in a thermometer manufacturer severe signs and symptoms of mercury poisoning. Complete disability developed insidiously over the last six months of employment. During the first two months of observation, the patient was treated in succession with three chelating agents: 2,3-dimercapto-l-propanol (BAL), D-penicillamine and sodium diethyldithiocarbamate (Dithiocarb). Each agent was administered initially for a period of approximately two weeks. A second course of therapy with BAL was administered for three days. Of the three complexing agents used, BAL gave the most dramatically favorable clinical response and yielded the highest urinary excretions of mercury. Dithiocarb was partially effective; d-pencillamine proved to be essentially ineffective. Analyses of the patient's sweat indicated that appreciable amounts of mercury were excreted by this route. Following the alleviation of the severe symptoms by BAL, the patient was placed on a regimen of daily sweats and physio-therapy for a protracted period of several months. On this latter regimen, the mercury levels in the urine, blood serum and sweat were decreased to within the normal ranges of values. The patient made a complete and uneventful recovery. In patients encountering psychotic and neurological disorders of undetermined etiology, consideration should be given to unsuspected or masked chronic exposure to mercury vapors as a possible cause.
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PMID:Clinical response to therapeutic agents in poisoning from mercury vapor. 21 Jul 2

For a number of years we have observed six patients whose illness began after inhaling high concentrations of mercury vapor in a single exposure. They all had symptoms of acute mercury poisoning with fever, chills, chest pain, and weakness. Three men had diffuse pulmonary infiltrates on chest x-ray suggesting chemical pneumonitis. Two of the men excreted large amounts of mercury in their urine two days after exposure following BAL therapy. Their chronic symptoms differed somewhat, but many complained of nervousness, irritability, lack of ambition, and loss of sexual desire. Chronic mercury poisoning is generally felt to follow only long periods of exposure. Although thess patients had symptoms which are not pathognomonic of chronic mercury poisoning, we feel the events described strongly suggest their relationship to a single brief exposure and represent a form of chronic mercurialism.
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PMID:Chronic mercury poisoning from a single brief exposure. 69 Jul 36

Micromolar concentrations of methylmercury and several organic mercury fungicides were found to block binding of [3H]acetylcholine (ACh) to the ACh-receptor of the electric organ of the electric ray, Torpedo ocellata. The same compounds had little or no effect on the catalytic activity of ACh-esterase of the same tissue. [14C]Methyl-mercury bound to the purified ACh-receptor with high affinity (Kd=7micrometer) and there were 6.5 +/- 0.5 binding sites for each ACh-binding site. Binding of methylmercury was highly cooperative with a Hill coefficient of 2.6. This binding was irreversible by redialysis in methylmercury - free medium, however, the bound [14C]methylmercury was easily displaced from the receptor protein with micrometer concentrations of BAL or penicillamine. Methylmercury also blocked binding of [3H] nicotine and [3H]pilocarpine to the nicotinic and muscarinic ACh-receptors of the rat brain, respectively. The data suggest that the ACh-receptor may be a target for methylmercury and other organic mercury compounds.
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PMID:Interactions of acetylcholine receptors with organic mercury compounds. 89 53

1 All five rats in a group survived if dimercaptosuccinic acid (DMSA), a water soluble derivative of 2,3-dimercaptopropanol (BAL), was given in doses of 10-40 mg/kg intraperitoneally 30 min, 4 and 24 h after administration of 2.4 mg/kg Hg as HgCl2, whereas three out of a group of five died if DMSA was not given. DMSA 20 mg/kg increased urinary excretion and decreased the body burden significantly more than 10 mg/kg DMSA, but further doubling of the dose had only marginal effects. 2 DMSA was able to reduce body burden and increase urinary excretion of Hg when intraperitoneal treatment started eight days after the subcutaneous administration of HgCl2. 3 DMSA was effective in decreasing body burden and the brain concentration of Hg in rats dosed orally with methylmercury (MeHgCl) when intraperitoneal treatment started with 40 mg/kg DMSA 24 h after Hg. Increase in the urinary excretion of mercury was responsible for the decrease in body burden. 4 DMSA was effective when given in the drinking water of rats or mice both against inorganic Hg and MeHgCl. In mice treated intraperitoneally with MeHgCl, DMSA 19.5 mug/ml in the drinking water caused a significant decrease in the body burden and increase in the excretion of Hg. 5 DMSA was about four times more efficient than D-penicillamine in decreasing the body burden of Hg. As their toxicity is in the same range, the higher efficiency of DMSA offers a larger margin of safety for the mobilization of Hg.
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PMID:The effects of dimercaptosuccinic acid on the excretion and distribution of mercury in rats and mice treated with mercuric chloride and methylmercury chloride. 126 Feb 28

The kinetics of oxygen penetration from the air into an oxygen free human BAL/saline and of its release from the oxygenated BAL/saline into a nitrogen environment was studied. Time-dependent oxygen concentration at constant temperature was monitored by recording the direct polarographic current of the second reduction wave of oxygen at a dropping mercury electrode. The obtained kinetic curves showed that not only uptake and release were quicker in BAL than in saline but also the corresponding equilibrium values were higher. Release and uptake curves in BAL were markedly different. The release was faster than the uptake but its maximal value was about 30% under the maximal uptake level. We suggest that the differences in oxygen uptake and release kinetics might contribute to explain the previously found accumulation of oxygen in BAL. The positive difference between the release and uptake kinetics at the beginning of the curves is consistent with a steady oxygen penetration through the BAL. The difference in the maximal oxygen uptake level and the maximal release level indicates a partial retention of the oxygen in the system.
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PMID:Oxygen penetration in and release from lung surfactant. 128 88

A woman ingested a dose of sublimate (approximately 0.9 g) in an attempted suicide. She survived and recovered in response to a combination of therapies including chelate (BAL) therapy, plasma exchange, haemodialysis and peritoneal dialysis. Serum inorganic mercury concentration, urinary inorganic mercury excretion and hair inorganic and organic mercury and selenium concentrations, along the length from the scalp to the distal part, were measured. Longitudinal analysis of hair, revealed a peak in inorganic mercury corresponding to the time of mercury ingestion. Organic mercury and selenium in the hair had different patterns of longitudinal variation from that of inorganic mercury. The biological half-life (23.5 d) of serum inorganic mercury levels was in good agreement with values previously reported in the literature.
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PMID:An acute mercuric mercury poisoning: chemical speciation of hair mercury shows a peak of inorganic mercury value. 135 62

Acute toxicity and the disposition of inorganic mercury depends on the route of exposure. Most previous studies on effect of chelators on inorganic mercury toxicity and toxicokinetics employed parenteral administration of both metal and chelator. However, the most prominent routes for human inorganic mercury exposure are the oral or pulmonary. BAL was previously considered the drug of choice in human intoxications with most heavy metals. This recommendation has been questioned during recent years due to the advent of the less toxic hydrophilic BAL analogues DMSA and DMPS. The present study, using oral administration of HgCl2 labelled with 203Hg, demonstrates that DMPS is superior to the other chelators in preventing mortality. Moreover, both DMSA and DMPS are superior to BAL and NAPA in alleviating acute toxicity and in preventing the undesirable distribution of orally administered mercury, especially to the brain. Further, oral administration of these chelators were more efficient than parenteral administration in reducing whole-body retention and organ deposition of orally administered mercuric chloride, most likely due to the prevention of intestinal uptake of mercury.
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PMID:Effect of four thiol-containing chelators on disposition of orally administered mercuric chloride. 168 54

At the very beginning of its migration pathway to any tissue, oxygen has to cross the lung surfactant surface layer (LSSL) and the underlying aqueous hypophase. The influence of human broncho-alveolar lavage and its lipid and specific protein components on oxygen transport were studied in vitro using sensitive electrochemical techniques. LSSL adsorbing from BAL at the dropping mercury electrode/saline interface shifted the peak potentials of oxygen reduction Ep towards more negative values. The magnitude of delta Ep was dependent on the quality of BAL. The kinetics of the oxygen transport were evaluated by measuring changes in the intensities of the reduction current. Storage of oxygen in BAL was several times higher than in saline and indicated the presence of one or more binding sites or promoters for oxygen among BAL components. The surfactant specific protein was found to be one of the binding sites (or promoters) for the oxygen. Since electron microscopic immuno-gold labelling demonstrated the presence of this protein in the LSSL, and electrochemically it proved to transport lipids from the surface layer to the subphase, it was suggested that Sp-A plays the role of an oxygen carrier.
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PMID:Oxygen transport through lung surfactant and the surfactant specific proteins. 209 66

The aim of our work was to establish the influence of the HgCl2 poisoning (various doses) on the Fe distribution in the rat organism. 175 Wistar rats were divided into 5 groups: I--control group, II--intoxicated with HgCl2 in the dose of 1 mg/kg of body weight, in the III group the HgCl2 dose was 6 mg/kg, in the IV group--12 mg/kg, in the V--12 mg/kg but rats of this group were given afterwards BAL (2.3-dimercaptopropanol). All rats were given 0.2 ml of 59FeCl3, radioactivity 3.7 kBq. The animals were put to sleep with chloroform after 3 and 6 hours, and 1, 2, 4, 8, 14 days after the isotope administration. For the radiometric assays the following organs or tissues were taken: stomach, small and large intestine, liver, kidneys, lungs, heart, muscles, spleen, blood, brain, testicles. The results are given in the percent of Fe dose in 1 g of wet tissue. The statistical analysis (Students' t test) was performed. The results indicate that in poisoned animals the Fe distribution was different than in controls. Increased concentration of 59Fe was noted after 3 and 6 hours in stomach and after 1 day in large intestine, whereas in other organs the Fe concentration was lower, correlating usually with the Hg dose. One interesting thing was noted: the Fe concentration in almost all organs was higher in rats intoxicated with the 12 mg/kg dose of HgCl2 and given afterwards BAL (IV group), than in rats that were not given BAL. Present results can have some practical significance in therapeutic procedure in mercury poisoning and during the convalescence.
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PMID:[Effect of mercuric chloride poisoning on iron distribution in rats]. 213 51


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