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)

Providencia stuartii was the most prevalent isolate recovered from urine specimens taken weekly over a 1-year period from 51 nursing home patients with urinary catheters in place. Thirty percent of the isolates were urease positive. Urease, which is implicated in renal stone formation, was shown to be transmissible on an 82-kilobase conjugative plasmid in one isolate. Plasmid DNA isolated from this strain was digested with EcoRI, ligated into the EcoRI site of pBR322, and used to transform Escherichia coli HB101. Ampicillin-resistant clones were replica plated onto urea segregation agar, and a urease-positive clone, designated pMID101, was isolated. Recombinant and native urease from cell lysates had identical electrophoretic mobilities on nondenaturing polyacrylamide urease activity gels. The native enzyme was induced fourfold when cells were grown in the presence of 0.1% urea and had a km of 9.4 mM and a Vmax of 3.2 mumol of NH3 per min per mg of protein. Its molecular weight was estimated to be 375,000 +/- 35,000 by Sephacryl S-300 chromatography. The enzyme was cytoplasmic in P. stuartii, was inhibited in vitro by hydroxyurea, acetohydroxamic acid, and EDTA, and appears to have a complex subunit structure and a unique molecular size within genera of the Proteeae tribe.
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PMID:Cloning of urease gene sequences from Providencia stuartii. 375 33

Ureolysis was investigated in salivary bacteria from persons with widely-differing oral ureolytic activities. Rate curves and product stoichiometry were established for urea disappearance, ammonia appearance and conversion of [14C]-urea to 14CO2. Ammonia, released stoichiometrically from urea, was best measured by a direct phenate-hypochlorite reaction. About 80 per cent of the urea-C was liberated as free CO2. Slight deviations from ammonia stoichiometry and most of the CO2 loss occurred in the first 5-10 min of reaction, when the rate of urea disappearance was constant and up to 2-fold higher than subsequently. This rate-change suggests that flux in the ureolysis pathway may be under feedback control. Ureolysis by salivary-sediment bacteria followed Michaelis-Menten kinetics with a Km of 2.5 mM; rates of end-product formation were independent of urea concentration between 25 and 500 mM. Ureolysis was inhibited 98 per cent by 5 mM acetohydroxamic acid, a urease inhibitor, and could be partly solubilized by sonication to give an enzyme preparation which, without cofactor supplementation, quantitatively hydrolysed urea. Thus urea metabolism by oral bacteria may principally involve urease-catalysed hydrolysis, rather than non-urease pathways.
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PMID:Kinetics and product stoichiometry of ureolysis by human salivary bacteria and artificial mouth plaques. 393 57

We present a study of the enzymatic activities involved in the pathway for arginine catabolism by Agrobacterium tumefaciens. Nitrogen from arginine is recovered through the arginase-urease pathway; the genes for these two activities are probably chromosomally born. Arginase was found to be inducible during growth in the presence of arginine or ornithine. Urease was constitutively expressed. Ornithine, resulting from the action of arginase on arginine, could be used as a nitrogen source via transamination to delta 1-pyrroline-5-carboxylate and reduction of the latter compound to proline by a reductase (both enzymatic activities are probably chromosomally encoded). Ornithine could also be used as a carbon source. Thus, we identified an ornithine cyclase activity that was responsible for direct conversion of ornithine to proline. This activity was found to be Ti plasmid encoded and inducible by growth in medium containing octopine or nopaline. The same activity was also chromosomally encoded in some Agrobacterium strains. In such strains, this activity was inducible during growth in arginine-containing medium.
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PMID:Arginine catabolism in Agrobacterium strains: role of the Ti plasmid. 395 72

In two experiments with one dairy cow each the utilisation of urea-N after its ruminal or duodenal infusion was comparatively investigated on two crude protein levels and different urease activities in the rumen. The rations contained 9.6 (I) and 14.3 (II) g crude plant protein/100 g dry matter. After completed adaptation 50 g urea were daily infused in the rumen (R, via cannula) in 3 h resp. the duodemun (D, distal cannula of the reentrance cannula) in 6 h with the morning and evening feeding. In experiment II the urease blocker phosphoric acid phenylester diamide (D/PPD) was applied in an additional experiment synchronously with the duodenal urea application. On the first measuring day in each case the urea in the morning feeding was labelled with 17.4 atom-% 15N-excess (15N'). Measuring results in the sequence I R, I D, II R, II D, II D/PPD: 15N'-passage rate at the duodenum within 72 h in the TCA-soluble N-fraction 29, 18, 24, 13 and 16, in the TCA-precipitable N-fraction 59, 25, 41, 11 and 5% of the application, 15N'-excretion within 96 h in milk protein 6.8, 4.2, 4.6, 3.4 and 1.9, in faeces 20, 12, 19, 8 and 4, in urine 20, 32, 34, 56 and 75% of the application, 15N-balance 59, 56, 47, 36 and 21% of the application, passage rate of non-NH3-N in the duodenum 131, 118, 96, 107 and 99% of the total N-intake. After ruminal infusion there always was a higher NH3-concentration in the rumen and 15N-frequencies in the rumen proteins. One can conclude that urea-N that gets into the intestines is to a low degree used for duodenal protein supply as directly utilisable urea-N from the ration in the rumen. The difference increases with the protein content of the ration and the inhibition of rumen urease. The urea N-balance is to a considerably smaller degree influenced by the place of urea infusion particularly at a low level of N-supply, which is due to a better utilisation of the urea-N transported with intermediary metabolism from the intestines. The role of urease as a regulator of urea transport through the rumen wall cannot be corroborated.
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PMID:[Transport of urea nitrogen from the intestines into the stomach in dairy cows]. 652 64

Biotransformation of NO, nitrite and nitrate was investigated in rats and mice in a 15NO inhalation experiment and intraperitoneal injection experiments of 15N-nitrite and 15N-nitrate, and the following results were obtained: (1) Rats were forced to inhale 15NO (145 ppm, 123 minutes) or were given an intraperitoneal injection of 15N-nitrite (2 mg animal-1 as 15N) or 15N-nitrate (2mg animal-1 as 15N), and determination of 15N recovery in urine was made up to 48 h later. The results were 55, 53 and 78% of the inhaled or injected 15N, respectively. (2) 15N-nitrate in the urine was converted into a 6-nitro derivative of 3,4-xylenol and its identification and quantitative determination were made by the GC-MS method. As to 15N-urea in the urine, identification and quantitative determination were made by the urease method. 15N was present in the urine of rats after 15NO inhalation in the form of NO3- and urea. 75 and 24% respectively. In the urine of rats injected with 15N-nitrite, about 20% of unidentified 15N-compounds not discovered in the inhalation experiment was found. The content of 15N-urea in the urine after injection with 15N-nitrate was lower than that after injection with 15N-nitrite. (3) When 15N-nitrite (0.617 mg animal-1 as 15N) was injected intraperitoneally in mice, 60.7, 7.8 and 0.3% of the injected 15N were found in the urine, feces and exhaled gas (NO, NO2 and NH3 in the gas were caught) up to 48 h after injection respectively, and 1.6% was found in the body 48 h after injection, but the remaining 30% of 15N could not be recovered.
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PMID:Biotransformation of nitric oxide, nitrite and nitrate. 662 3

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

After a brief review of the methods for determination of urea by continuous flow analyzers, a method is described based on the urease splitting of urea followed by NH3 reaction with alfa-ketoglutarate + NADH2 catalysed by GLDH. The method has been applied to continuous flow analyzers and seems to be promising.
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PMID:[Review of the methods of determination of blood urea with continuous-flow analyzers and a proposal of a completely enzymatic UV method for urea by a continuous-flow analyzer]. 718 46

An amount of 0, 0.1, 0.5 and 1.0% (related to N) of phosphoric phenyl ester diamide (PPD) effective as urease blocking substance was applied to the surface of urea with oilbitumen and fed to cows with rumen cannulae over a period of 31 resp. 164 ... 167 days. (The ration essentially consisted of 4.5 kg dried roughage and 1.5 kg starch or 1.1 kg starch plus 0.4 kg sugar and contained 50 g urea). By treating the urea with PPD, the activity of urease, the hydrolysis rate of urea and the NH3-concentration in the rumen were significantly diminished 0.5 to 2 hours after feeding (alpha = 0.05). The effect of PPD was greatest in the first days and decreased with the advancing feeding period. In the variant with 0.5% PPD the examined parameters were significantly reduced after 142 to 164 days, too. This effect remained traceable in its diminished form even after the preparation was discontinued over a period of 35 days. The dynamics of the NH3-concentration was not altered by PPD after a longer feeding period. One can conclude that PPD inhibits the hydrolysis of urea but does not retard it. In conclusion one can say that, because of PPD, the toxicity of urea is lower without the utilisation of urea being better. Due to PPD the molar propionate level in volatile fatty acids decreases significantly and the acetate-propionate relation is expanded.
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PMID:[Studies on the effect of phosphoric phenyl ester diamide as inhibitor of the rumen urease of dairy cows. 1. Influence on urea hydrolysis, ammonia release and fermentation in the rumen]. 728 28

Two lactating dairy cows supplied with rumen and duodenal re-entrance cannulae received with their rations containing 8.2% vegetable crude protein 180 g urea per day (I) or urea treated with the urease inhibitor phosphoric phenyl ester diamide (PPD, 1% of the N-quota). The cows, accustomed to urea, received the PPD-urea without adaptation (II) and after a 30-day adaptation (III) to PPD. On the first day of the experiment one half of the urea was given ruminally in its 15N-labelled form. 2 h after the isotope supplementation 62.5 and 24 mg NH3 and 6.58 and 21 mg urea/100 ml could be detected in the rumen juice of I to III. Within 72 h 16.6, 26.1 and 25.2% of the 15N-excess given (15N') passed the duodenum in TCA - soluble form and 31.2, 28.4 and 41.7% in TCA - precipitable form. 15.6, 24.4 and 21.5% of the total amount of 15N were excreted in urine and 4.5, 4.6 and 6.0% in the milk protein. The values for faeces were 14.4, 14,4 and 15.4%. The conclusion from these results and from the dynamics of the relative 15N' in the fractions of the rumen fluid is that with a limited inhibition of rumen urease by PPD as it develops after the adaptation, the utilisation of urea-N can be improved.
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PMID:[Studies on the effect of phosphoric phenyl ester diamide as inhibitor of the rumen urease of dairy cows. 2. The metabolism of 15N-urea]. 728 29

The factors that determine which Helicobacter pylori infected subjects develop duodenal ulcer (DU) are unclear. This study tested the hypothesis that infection density and urease activity are higher in DU than non-DU subjects. Fifty five DU and 55 age and sex matched non-DU subjects were studied. Quantitative methods were used for measuring infection density (viable organism count) and urease activity (Berthelot reaction). DU subjects had a greater antral infection density (geometric mean of colony forming units/mg biopsy protein; 10.5 x 10(5) v 1.3 x 10(5), p < 0.001). They also had higher biopsy urease activity (geometric mean of NH3 nmol/min-1/mg protein-1; 103 v 25, p < 0.001). Urease activity per organism, however, was similar in the two groups showing that high antral urease activity in DU was a reflection of organism density. DU was not present in subjects with an antral infection density less than 10(5) colony forming units/mg protein. A correlation was present between H pylori viable counts and the severity and activity of gastritis. Both severity and activity of gastritis were greater in the antrum of DU compared with non-DU subjects but there was no difference in the body between the two groups. It is concluded that antral H pylori infection density is probably an important determinant of DU development, and that there is a baseline of infection density that is necessary for ulcer formation.
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PMID:Helicobacter pylori infection density and gastric inflammation in duodenal ulcer and non-ulcer subjects. 870 3


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