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)

Endolysin was induced in Pseudomonas BAL-31 infected with bacteriophage PM2 and was also associated with the purified virion. This enzyme required divalent cations for its activity, Ca2+ being the most effective cation. Endolysin activity in the virion increased up to three-fold upon disruption and the activity could be localized in the viral nucleocapsid. Thus the enzyme is localized within the virion. After purification of the structural proteins of bacteriophage PM2, only the nucleocapsid protein (III) had endolysin activity.
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PMID:Structure and synthesis of a lipid-containing bacteriophage. An endolysin activity associated with bacteriophage PM2. 89 52

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

Initial experiments involving mouse development employed single IP injections of 45 mg/kg sodium arsenate on one of days 6-12 of gestation and produced a spectrum of developmental defects. Embryotoxicity was indicated by high prenatal mortality and decreased fetal weights. A chelating agent, 2,3-dimercaptopropanol (BAL), was then employed in an attempt to alleviate the adverse effects of prenatal arsenate. BAL was administered 4 hr before, concurrently with, or 4 hr after arsenate. All BAL treatments diminished arsenate-induced gross malformations and growth retardation; the concurrent treatment alleviated skeletal malformation. Injection of rats IP with arsenate has also been reported to result in teratogenicity, including renal agenesis. Further reports indicated that 40 mg/kg arsenate administered to mice by gavage on days 9-11 increased prenatal mortality, reduced fetal weights, and was associated with minor malformations. According to our recent work, however, single oral doses of arsenate must be around 120 mg/kg to cause prenatal toxicity. Multiple doses of 60 mg/kg on 3 days had little effect. Sodium arsenite has also been found to be fetotoxic and teratogenic. Such effects were seen at IP doses of 10-12 mg/kg.
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PMID:Effects in the mouse and rat of prenatal exposure to arsenic. 90 2

The highly single strand-specific extracellular nuclease of Pseudomonas BAL 31 is shown to cleave non-supercoiled closed circular duplex PM2 bacteriophage DNA containing regions of altered helix structure produced in vitro by irradiation with ultraviolet light or by treatment with the carcinogen, N-acetoxy-N-2-acetylaminofluorene. Untreated samples of this DNA are affected very little by the nuclease. The unwinding of the DNA helix associated with the above treatment renders the closed circular DNA positively supercoiled compared to untreated samples. The extent of unwinding can be accurately measured and correlated with the average number of lesions per molecule of DNA by monitoring the alterations of the electrophoretic patterns, relative to those observed for untreated DNA, of such DNA in agarose gels. Interstrand cross-links and mismatched base pairs produced by treatment of non-supercoilded circular duplex DNA with the mutagen, nitrous acid, do not detectably unwind the DNA helix. The nitrous acid-treated DNA provides substrates for cleavage by the Pseudomonas nuclease which are likely to be the interstrand cross-links rather than the mismatched base pairs. Use of the Pseudomonas nuclease in conjunction with agarose gel electrophoresis can provide a powerful method for the detection of damage in duplex DNA such as that introduced by carcinogenic and mutagenic agents.
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PMID:A sensitive endonuclease probe for lesions in deoxyribonucleic acid helix structure produced by carcinogenic or mutagenic agents. 92 19

Among 15 chelating agents tested, sodium-2,3-dimercaptopropane 1 sulfonate (DMPS), 2,3-dimercaptopropanol (BAL), sodium-mercaptoethyliminodiacetate (MEIDA), and D-penicillamine (PA) exerted an influence on the excretion of Hg and its distribution in the organs. The excretion pattern however, is different for these compounds, and, from the practical point of view, a favourable effect is exhibited only by DMPS which enhances the urinary excretion rate and lowers the Hg-concentration in all organs.
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PMID:The excretion and distribution of inorganic mercury in the rat as influenced by several chelating agents. 94 4

The angiotensinase inhibitor 2,3-dimercaptopropanol (BAL) interferes with peptide-antibody binding when certain sensitive antisera are used in angiotensin I radioimmunoassay systems. Three of nine antisera tested showed sufficient interference to produce serious errors in data obtained using these antisera together with BAL. For PRA determinations in human plasma, at both pH 5.7 and pH 7.3, relationships between different PRA'S are altered, and results of renin stimulation tests are changed in unpredictable ways. Determination of renin concentration in rat plasma does not require use of BAL as inhibitor, and it is best avoided. For human plasma renin determinations, use of BAL-sensitive antisera should be avoided, since there is no satisfactory way to correct data for the resulting error. BAL itself, rather than its oxidation products, is probably the interfering substance. The interference appears to be due to an interaction between BAL and the BAL-sensitive antiserum. It is not related to the known actions of BAL as chelating or reducing agent.
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PMID:Interference by 2, 3-dimercapto-1-propanol (BAL) in angiotensin I radioimmunoassay. 95 83

Infection of Pseudomonas BAL-31 with the lipid-containing bacteriophage PM2 resulted in no detectable change in the rate of phosphatidylglycerol (PG) or phosphatidylethanolamine (PE) biosynthesis. An increase in the PG content of infected cultures was not seen until the cultures began to lyse, and this increase was in fact only a relative increase resulting from the extensive turnover of PE at the onset of culture lysis. Turnover studies revealed that the glycerol, phosphorus fatty acid, and ethanolamine moieties of PE turned over simultaneously at the time of lysis, and therefore made it unlikely that there was a PE to PG conversion during the latent period of the phage. The lipid found in the bacteriophage did not reflect a preferential selection for lipid synthesized before or after infection, but in fact reflected the composition of the host membrane at the time the phage were assembled. The use of a modified medium that allowed the cultivation of Pseudomonas BAL-31 as a prototroph and resulted in reliable lysis times of infected cultures led us to the conclusion that PM2 infection effects little change in host phospholipid metabolism, and that there is sufficient PG in the host cytoplasmic membrane to account for a full burst of phage. As a result of the reliable lysis times that we have achieved, we concluded that certain metabolic events, i.e., PE turnover, are lytic phenomena and must not be confused with events relevant to the biosynthesis and maturation of the phage.
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PMID:Phospholipid metabolism in Pseudomonas BAL-31 infected with lipid-containing bacteriophage PM2. 95 79

Compound X, a minor phospholipid of Pseudomonas BAL-31 and bacteriophage PM2, has been identified as X-3-phosphatidyl-1'-(3'-acyl)-glycerol, or acyl phosphatidylglycerol. The water-soluble product obtained by mild alkaline hydrolysis showed the same RF value as that of glycerophosphoryl-glycerol. The chemical analysis gave the ratio 1 : 3 : 2 for phosphate-acyl ester-glycerol. The position of the third acyl group was determined by nuclear magnetic resonance techniques.
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PMID:Identification of acyl phosphatidylglycerol as a minor phospholipid of Pseudomonas BAL-31. 99 Feb 98

The electrophoretic mobility of renin substrate in human plasma was determined by electrophoresis of the plasma on a cylinder of polyacrylamide gel, followed by slicing the gel, incubation of each slice with human renin, EDTA, and BAL in saline, and determination of the angiotensin formed by radioimmunoassay. With this modified technique 5, and possibly 8, electrophoretically dissimilar renin substrates have been found in human plasma. Significant variations in the patterns of renin substrates in the blood plasma of pregnant women and of those taking oral contraceptives were shown. In normal plasma from male or female subjects there was a single large peak of renin substrate with a mobility slightly less than that of albumin, and there were a series of very small peaks of renin substrate with lesser mobilities than the major peak. Increasing the sample size and prolonging the period of incubation with renin made the smaller peaks more apparent. In women using oral contraceptives, a distinctly different pattern of renin substrates was found. Early smaller peaks were increased. The major peak was sometimes increased also. Pregnancy produced a strikingly different pattern of renin substrates. There was an increase in all slow-moving peaks and their bases ran together without a return to the baseline. The absence of peaks when renin was omitted indicated that they were renin substrates. In 2 of 4 patients having cirrhosis of the liver with ascites, the amount of major substrate peak was greatly diminished and minor peaks were somewhat reduced. In 3 bilaterally nephrectomized patients, the major peak was not increased and the pattern of minor peaks was normal.
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PMID:Heterogeneity of renin substrate in human plasma: effect of pregnancy and oral contraceptives. 99 64

Rapid and progressive inactivation in vitro of both alcohol dehydrogenase and aldehyde dehydrogenase by low concentrations of acetaldehyde or formaldehyde is illustrated. This inactivation can be prevented or reversed by glutathione or other SH reagents. Those effects led to investigations in vivo. Rats and mice were injected with concentrations that would result in death in approximately 10 h (methanol) and approximately 4 h (formaldehyde). When 2,3-dimercaptopropanol (BAL), cysteine, or mercaptoethanol was injected (10 min to 3 h) after administration of methanol or formaldehyde, approximately 70% of the animals survived indefinitely; the remaining 30% showed substantial increase in survival time. The findings indicate the possibility of using reagents such as BAL for human therapy and suggest that the toxicity of methanol and formaldehyde is due in part to effects other than acidosis.
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PMID:Protection against toxic effects of formaldehyde in vitro, and of methanol or formaldehyde in vivo, by subsequent administration of SH reagents. 102 22


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