Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sorbyl-, benzoyl-, and 3-amino-benzoyl hydroxamic acids inhibited the development of an alkaline pH by T-strain cultures grown in broth containing 0.05% urea and phenol red. The specificity of this urease inhibition was demonstrated by the inhibition, by 10(-4)m sorbyl-hydroxamic acid, of the release of (14)CO(2) from (14)C-urea by washed T-strain mycoplasmas in 4 hr of incubation. Sorbyl-, benzoyl-, and 3-amino-benzoyl hydroxamic acids at a concentration of 10(-3)m markedly inhibited the multiplication of T-strain 354 during 18 hr of incubation; this inhibition was not corrected by thymidine at a concentration of 500 mug per ml. Aurothiomalate was 20 times more inhibitory to Mycoplasma hominis DC-63 than to T-strain 354; equivalent inhibitory concentrations were 50 mug per ml for M. hominis and 1,200 mug per ml for T strains.
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PMID:Inhibition of growth of T-strain mycoplasmas by hydroxamic acids and by aurothiomalate. 420 56

Color change of pH indicators in broth medium is commonly used to quantify growth of ureaplasmas. These organisms differ from other members of the Mollicutes by their ability to hydrolyze urea to CO2 and NH3. This study describes a method which continuously monitors color change in ureaplasmal broth cultures. Using this technique we found: (i) there was a pH-dependent absorbance at 554 nm in ureaplasmal broth medium containing phenol red, (ii) a sigmoidal-shaped color changing curve (absorbance at 554 nm versus time) was produced by metabolizing organisms whereas a linear curve was generated by antibiotic-inhibited ureaplasmas, and (iii) the minimum cell density which elicited a growth-inhibited color change was 1.25 x 10(4) colony-forming units per ml. Other have shown that apparently dead ureaplasmas can cause a color change in broth media. This color change is probably due to the presence of an active urease. This study graphically and quantitatively assesses growth-inhibited color change.
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PMID:Effect of antibiotics on the dynamics of color change in Ureaplasma urealyticum cultures. 701 6

Two complementing loci in different linkage groups of the basidiomycete Ustilago violacea are involved in urease activity: a structural one (ure-1) and a second inferred to involve a permease (ure-2) locus. Two types of complementing mutations occur in the structural locus: null activity (ure-la) and obviously reduced activity (ure-1b). The ure-2 mutants lacked urease activity in vivo on the phenol red-urea est medium, but gave extracts with wild-type activity. Extracts from wild-type strains gave one site of urease activity after polyacrylamide gel electrophoresis. A number of ure-1b mutants and activity revertants from ure-1a mutants yielded electrophoretically variant urease sites. The results are discussed in terms of enzyme polymorphism in haploid eukaryotes by one (missense) or two (null, then missense) mutations.
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PMID:The genetics and biochemistry of urease in Ustilago violacea. 733 90

Urea is extracted from rodent urine-contaminated material with hot acetone. After the extract is evaporated to dryness, aqueous urease solution is added to produce ammonia and carbon dioxide. A blue product, indophenol, is formed by the reaction of ammonia with phenol in the presence of hypochlorite. Absorbance is maximum at 625 nm. Presence of urea is easily detected at 4 microgram. Detection of urine contamination in various materials is compared with detection by the AOAC urease-H2PtCl6 test.
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PMID:Spectrophotometric determination of urea in urine stains on foods and containers. 741 Mar 9

Helicobacter pylori urease is a nickel-containing enzyme that hydrolyzes urea to bicarbonate and ammonia. Andrews et al. (J. Am. Chem. Soc. 1986, 108, 7124) have shown that amides and esters of phosphoric acid are slow, tight-binding inhibitors of urease isolated from jack bean. We show that 4-substituted phenyl phosphorodiamidates (4-R-PhOP(=O)(NH2)2) are slow-binding inhibitors of H. pylori urease with no evidence of kinetic saturation. Their second-order rates of inhibition ki are strongly correlated with phenol pKa (e.g. R = NO2, ki = 2.5 x 10(5) M-1s-1; R = OMe, ki = 1.2 x 10(4) M-1s-1). The Bronsted beta for inhibition is 0.4, similar to that of model system SN2(P) reactions. Based on these observations, we suggest that urease inhibition is covalent but reversible, involving a common phosphoacyl enzyme intermediate.
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PMID:Inhibition of Helicobacter pylori urease by phenyl phosphorodiamidates: mechanism of action. 764 8

Forty-nine patients with Helicobacter pylori (Hp)-positive gastric ulcer (GU) and 39 patients with Hp-positive duodenal ulcer (DU) were studied. Before the trial and every 3 or 4 weeks, phenol red dye spraying endoscopy, the rapid urease test, biopsy specimen histology, and culture were performed to assess the ulcer stage and to detect Hp. Patients were divided into three groups: group I received lansoprazole 30 mg/d; Group II received dual therapy of lansoprazole 30 mg/day and amoxicillin (AMPC) 1 g/day or clarithromycin (CAM) 400 mg/day; and Group III received combination therapy of lansoprazole 30 mg/day, AMPC 1 g/day, or CAM 400 mg/day, and metronidazole 500 mg/day. Patients with GU received lansoprazole for 8 weeks and patients with DU received lansoprazole for 6 weeks. The other agents were administered for 2 weeks at the beginning of the trial. There were no differences in ulcer healing among the three treatment groups in patients with GU or DU, but there were significant differences in the eradication of Hp. No side effects were observed in any of the patients. We conclude that combination therapy is likely to be most effective and is harmless for Hp-persistent patients with peptic ulcer.
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PMID:Lansoprazole treatment of Helicobacter pylori-positive peptic ulcers. 767 15

The effects of yogurt containing viable Lactobacillus strain GG (L. GG) and/or fiber supplements on fecal enzyme activities (beta-glucuronidase, nitroreductase, beta-glucosidase, glycocholic acid hydrolase, urease) and on bacterial metabolites in urine (phenol, p-cresol) were studied in 64 females, 20-41 y old. The subjects were randomly divided into three groups: the first group received L. GG yogurt (2 x 150 mL/d, containing 10(11) colony-forming units (cfu)/L of L. GG), the second group received L. GG yogurt and a rye fiber product (30 g/d, equivalent to 9 g fiber/d), and the third group received placebo yogurt (pasteurized) and fiber. The supplementation period lasted 4 wk, with a preceding 2-wk baseline period and a 2-wk follow-up period. The mean fecal count of L. GG was approximately 10(6) cfu/g feces during the supplementation, and L. GG persisted in the fecal samples of 28% of the subjects for 2 wk after supplementation. L. GG yogurt alone or with fiber significantly decreased fecal beta-glucuronidase, nitroreductase and glycocholic acid hydrolase activities. These enzyme activities returned to baseline levels during the follow-up period. beta-Glucosidase and urease activities were not altered significantly during the study. The addition of fiber to L. GG and placebo yogurt had no effect on the enzymic activities. Urinary excretion of p-cresol decreased significantly in groups receiving L. GG. These data demonstrate that L. GG can modify the colonic environment with possible health effects.
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PMID:Lactobacillus strain GG supplementation decreases colonic hydrolytic and reductive enzyme activities in healthy female adults. 828 90

To evaluate the sensitivity of a polymerase chain reaction (PCR) assay using nested primers in detecting Helicobacter pylori, gastric tissue biopsy specimens were collected on endoscopy from 17 patients with a duodenal ulcer. DNA was extracted by phenol/chloroform treatment or boiling in water, and then subjected to a nested PCR using two primer pairs from the urease gene of Helicobacter pylori. Fourteen of the 17 patients were positive for Helicobacter pylori using DNA samples extracted by either method. The PCR results correlated well with the results of an enzyme immunoassay to detect IgG antibody. However, there were two culture negative patients. The three PCR negative patients were both culture negative and serologically negative. DNA from 9 of the 14 patients was randomly selected and subjected to semiquantification by serial dilutions, and then PCR. The results showed that phenol/chloroform extraction yielded 10-1000 times more DNA than the boiling method. It is concluded that the PCR assay is a rapid and sensitive method for detecting Helicobacter pylori, and that phenol/chloroform extraction is superior to simple boiling in obtaining DNA samples for PCR.
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PMID:Detection of Helicobacter pylori in gastric biopsy tissue by polymerase chain reaction. 835 5

A bacterial strain that was able to mineralize 2,4,6-trichlorophenol was isolated from a chlorophenol-fed percolator and was identified as a member of the genus Rhodococcus on the basis of chemotaxonomic characteristics and 16S RNA phylogenetic inference data. This organism (strain MBS1T [T = type strain]) exhibited a typical irregular rod-coccus cycle, and the cells had fimbria-like structures on their surfaces. The diagnostic cell wall amino acid was meso-diaminopimelic acid, and the sugars were arabinose and galactose; the mycolic acids contained 46 to 54 carbon atoms. The main menaquinone was MK-8(H2), and MK-9(H2) was a minor component. The cellular phospholipids were phosphatidylethanolamine, phosphatidylinositol, phosphatidylinositolmannoside, phosphatidylglycerol, and diphosphatidylglycerol. Tuberculostearic acid was present. The whole-cell fatty acids were straight-chain acids with 14 to 18 C atoms. The G+C content of the DNA was 67.4 mol%. This organism grew on sucrose, pyruvate, and 2,4,6-trichlorophenol, and it oxidized a large number of carbon compounds, including catechol, 3-hydroxyphenylacetic acid, and phenol. It also exhibited beta-galactosidase, urease, and 2-acetyl-lactate decarboxylase activities. On a phylogenetic tree that was based on 16S ribosomal DNA gene sequences strain MBS1T was found among the rhodococci on an independent branch. On the basis of the chemotaxonomic and phenotypic characteristics of strain MBS1T and its phylogenetic position we suggest that this bacterium should be placed in a new species, Rhodococcus percolatus; the specific epithet was chosen because the organism was isolated by using an enriched percolator. The type strain is strain MBS1.
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PMID:Rhodococcus percolatus sp. nov., a bacterium degrading 2,4,6-trichlorophenol. 857

A number of diagnostic tests have been developed for the detection of H. pylori. Diagnostic techniques can be divided into invasive and noninvasive methods. The invasive methods require upper gastrointestinal endoscopy and involve culture of gastric biopsy specimens, examination of stained biopsies and detection of urease activity in the biopsies themselves. In addition, we have developed endoscopic diagnosis of H. pylori infection in gastric mucosa using phenol red dye-spraying. The noninvasive methods include urea breath test and serological techniques. Although there has been considerable improvement in the techniques, a combination of at least two different techniques should be used in order to optimize the diagnostic yield. We recommend the use of one rapid test in the combination. The rapid urease test, cytology and the phenol red dye-spraying endoscopy give results available before the patient leaves the endoscopy suite.
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PMID:Diagnosis of Helicobacter pylori infection. 884 Feb 43


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