Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microbioassays using bacteria or enzymes are increasingly applied to measure chemical toxicity in the environment. Attractive features of these assays may include low cost, rapid response to toxicants, high sample throughput, modest laboratory equipment and space requirements, low sample volume, portability, and reproducible responses. Enzymatic tests rely on measurement of either enzyme activity or enzyme biosynthesis. Dehydrogenases are the enzymes most used in toxicity testing. Assay of dehydrogenase activity is conveniently carried out using oxidoreduction dyes such as tetrazolium salts. Other enzyme activity tests utilize ATPases, esterases, phosphatases, urease, luciferase, beta-galactosidase, protease, amylase, or beta-glucosidase. Recently, the inhibition of enzyme (beta-galactosidase, tryptophanase, alpha-glucosidase) biosynthesis has been explored as a basis for toxicity testing. Enzyme biosynthesis was found to be generally more sensitive to organic chemicals than enzyme activity. Bacterial toxicity tests are based on bioluminescence, motility, growth, viability, ATP, oxygen uptake, nitrification, or heat production. An important aspect of bacterial tests is the permeability of cells to environmental toxicants, particularly organic chemicals of hydrophobic nature. Physical, chemical, and genetic alterations of the outer membrane of E. coli have been found to affect test sensitivity to organic toxicants. Several microbioassays are now commercially available. The names of the assays and their basis are: Microtox (bioluminescence), Polytox (respiration), ECHA Biocide Monitor (dehydrogenase activity), Toxi-Chromotest (enzyme biosynthesis), and MetPAD (enzyme activity). An important feature common to these tests is the provision of standardized cultures of bacteria in freeze-dried form. Two of the more recent applications of microbioassays are in sediment toxicity testing and toxicity reduction evaluation. Sediment pore water may be assayed directly or solvents may be used to extract the toxicants. Some of the solvents used for extraction of organic chemicals are themselves toxic to bacteria (e.g., dichloromethane), requiring exchange with a less toxic solvent (e.g., ethanol, methanol, DMSO). A modification of the Microtox test allows direct assay of solid-phase samples such as sediments. The toxicity reduction evaluation (TRE) must be carried out at wastewater treatment plants whose effluents fail toxicity standards. The TREs require numerous and repeated toxicity assays, thus favoring application of microbioassays. Presently, no single microbioassay can detect all categories of environmental toxicants with equal sensitivity. Therefore, a battery of tests approach is recommended. The differential sensitivity of alternative tests may, in fact, be exploited. Further research is needed to construct strains of genetically engineered microorganisms or isolate microorganisms or enzymes that respond to specific classes of toxicants. These can be combined into batteries appropriate for different environments or test objectives.
 ...
PMID:Bacterial and enzymatic bioassays for toxicity testing in the environment. 150 75

Helicobacter pylori (HP) has been shown to possibly be a pathogen of gastric carcinoma. HP has urease activity and produces ammonia in the stomach. In this study, the role of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in rats. After 24 weeks pretreatment with MNNG (83 mg/l), 0.01% ammonia or tap water as a drinking water was administered for 24 weeks. The ammonia-treated rats showed a significantly higher incidence of gastric cancer (percent of animals with tumors and number of tumors per rat). Ammonia would thus appear to have an important role in HP-related human gastric carcinogenesis.
 ...
PMID:Ammonia: a possible promotor in Helicobacter pylori-related gastric carcinogenesis. 151 5

A prospective case controlled study was conducted to evaluate the role of fluoride as a possible aetiological factor for non-ulcer dyspepsia (NUD). Twenty patients with NUD and 10 age and sex matched healthy controls were subjected to clinical evaluation, upper gastrointestinal endoscopy and biopsies from the gastric antrum and duodenum. The antral and duodenal mucosa was subjected to a rapid urease test for Helicobacter pylori and histological and electron microscopic examinations. Fluoride levels in the drinking water, serum and urine were estimated using a ION 85 ion-analyser. These levels were significantly higher in patients with NUD than in controls (P less than 0.05). Histological abnormalities in the antral and duodenal mucosa were seen in 14 patients (70%) with NUD and 1 control subject (10%) (P less than 0.05). Electron microscopic abnormalities in the mucosal cells were seen in all patients with NUD but in none of the controls (P less than 0.01). The fluoride levels in serum and urine correlated with the symptoms, histological and electron microscopic abnormalities (P less than 0.05). It was concluded that chronic exposure to fluoride may result in NUD and should be considered in patients where other known cause of dyspepsia have been excluded.
 ...
PMID:Fluoride as a possible aetiological factor in non-ulcer dyspepsia. 151 58

To evaluate partial or total replacement of renal function using gut, we measured in vivo transport of nitrogen metabolites, electrolytes, and water into a jejunal segment configured as a continent reservoir in the dog. Reservoir contents were sampled and analyzed at serial time intervals during a 3-h period after instillation of solution containing (in mM) 40 NaCl, 10 NaHCO3, 220 mannitol, pH 8.5, without or with added urease. At 10 min postinstillation, the amount of urea in the solution without added urease was 3-5 times greater than in the presence of added urease, but accumulation of NH4+ was 14-21 times greater in the solution containing added urease, giving a luminal NH4+ concentration up to 10,000 times that of plasma. In the absence of urease, HCO3- concentration fell to 0, and pH declined to 6 at 3 h; in the presence of urease, HCO3- concentration was 4.5 mM, and pH was 7.8 at 3 h. We conclude 1) urea is secreted by the reservoir; 2) H+ is secreted and/or formed in the reservoir; 3) in the presence of urease, urea hydrolyzed to NH3 is converted to NH4+ by H+ and trapped in the lumen; and 4) in the urease solution, H+ binding by NH3 preserves luminal HCO3-, maintaining the initial pH. Thus the continent jejunal reservoir may supplement or replace impaired renal function.
 ...
PMID:Transport properties of an in situ jejunal reservoir in dogs. 155 68

Struvite (MgNH4PO4.6H2O) crystals, the major mineral component of infectious urinary calculi, were produced in vitro by growth of a clinical isolate of Proteus mirabilis in artificial urine. P. mirabilis growth and urease-induced struvite production were monitored by phase contrast light microscopy and measurements of urease activity, pH, ammonia concentrations, turbidity, and culture viability. In the absence of pyrophosphate, struvite crystals appeared within 3-5 h due to the urease-induced elevation of pH and initially assumed a planar or 'X-shaped' crystal habit (morphology) characteristic of rapid growth. When pyrophosphate was present, initial precipitation and crystal appearance were significantly impaired and precipitates were largely amorphous. When crystals did appear (usually after 7 or 8 h) they were misshapen or octahedral in shape indicative of very slow growth. X-ray diffraction and Fourier transform infrared spectroscopy (FTIR) identified all crystals as struvite. Trace contaminates of carbonate-apatite (Ca10(PO4)6CO3) or newberyite (MgHPO4.H2O) were produced only in the absence of pyrophosphate. P. mirabilis viability and culture pH elevation were unaffected by the addition of pyrophosphate, whereas urease activity and ammonia concentrations were marginally reduced. Struvite could also be produced chemically by titration of the artificial urine with NH4OH. If pyrophosphate was present during titration, the same inhibitory effect on crystal growth occurred, so it is unlikely that urease inhibition is important. Lowering of pyrophosphate concentration from 13-0.45 mumol/l did not reduce its inhibitory activity so it is unlikely to act by chelating free Mg2+. We propose that pyrophosphate inhibits struvite growth principally through direct interference with the chemical mechanisms involved in crystal nucleation and growth, because of its effectiveness at very low concentrations.
 ...
PMID:Pyrophosphate inhibition of Proteus mirabilis-induced struvite crystallization in vitro. 166 44

Under the term "non-calcium nephrolithiasis", three types of renal stone formation are considered. (1) Infected nephrolithiasis, which is due to bacteriological ureolysis. Its treatment includes lowering of oversaturation by antibiotics, urease inhibition and/or acidification of the urine; lowering of crystallization by eradicating concomitant infections caused by non-ureolytic organisms; prevention of crystal adherence by exogenous glycosaminoglycans, and prevention of bacterial adherence by glycolipids. (2) Uric acid lithiasis is defined on physico-chemical and physiopathological grounds. Medical treatment consists of increasing water intake, reducing puric acid intake, alkalinizing the urine inhibiting xanthine-oxidase. (3) Cystinuria is described as a nephrolithogenic proximal tubulopathy. Medical treatment includes reduction of urinary cystine concentration by a strong increase of water intake; reduction of urinary cystine excretion by diet and increase of cystine solubility by urinary alkalinization or administration of some thiol compounds.
 ...
PMID:[Physiopathology, etiology and medical treatment of non-calcium lithiasis]. 178 96

Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 +/- 2.2 for controls vs. -8.7 +/- 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24% increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.
 ...
PMID:Urease and the acidosis of urinary intestinal diversion. 185 52

A flow injection method was developed, aimed at the determination of urea in human serum. The system makes use of the naturally immobilized urease present in Canavalia ensiformis DC (jack bean). A column is filled with small pieces of this bean, and the sample (50 microliters) containing urea passes through it carried by a 1% NaCl solution. On leaving the column the stream is merged with an alkaline reagent (0.5 mol dm-3 NaOH; 0.5% disodium dihydrogen ethylenediaminetetraacetate). The ammonium ions, arising from the enzymatic reaction that occurs inside the column, are changed into the molecular form, which permeates a polytetrafluoroethylene membrane and is received in a de-ionized water acceptor stream. The ammonia ionizes causing an increase in the conductance, which is proportional to the urea content of the sample. About 40 samples can be processed in 1 h with negligible carry-over and with a relative standard deviation of 1% or less. The results are in agreement with those obtained by a standard spectrophotometric method.
 ...
PMID:Determination of urea in serum by using naturally immobilized urease in a flow injection conductimetric system. 187 83

H. pylori is a highly virulent organism as evidenced by its low infective dose and widespread high prevalence in human populations. Its virulence is achieved through its ability to survive in a moist environment and its massive urease production which allows it to survive in the acidic gastric juice long enough to colonize the gastric mucus. Gastric colonization is facilitated by cell wall associated lectins which permit the bacterium to bind to gastric mucus and the gastric epithelial cell. Once in this location, H. pylori produces several enzymes which may harm the gastric epithelium, particularly urease (through ammonia generation) and phospholipases A and C. H. pylori also weakens the gastric mucous layer by digesting its glycoproteins and lipids, making the mucus less hydrophobic and more water soluble. Helicobacter pylori attracts phagocytic cells, inducing both acute and chronic inflammation as well as an antibody response. Persistence of H. pylori in the mucosa may be enhanced by its cytotoxin and catalase production, by which it survives after phagocytosis by neutrophils.
 ...
PMID:Virulence and pathogenicity of Helicobacter pylori. 191 16

The prevalence of Helicobacter pylori (HP) in the gastric mucosa of patients with chronic atrophic gastritis has been reported to be significantly higher than in normal mucosa. To clarify the role of HP in the etiology of chronic atrophic gastritis, we assessed the effect of ammonia on the gastric mucosal structure in rats, since HP has a strong urease activity and produces abundant amounts of ammonia. Ammonia administered orally at 0.01% and 0.1% as drinking water for two to four weeks decreased the mucosal thickness and the parietal cell number and oxyntic gland number in a dose- and time-dependent manner. The decrease of mucosal thickness was significantly greater in the antral mucosa than in the body mucosa. The border between the antral and body mucosa shifted toward the cardia, reflecting the decrease in oxyntic gland numbers. Furthermore, intracellular mucin was also decreased in a dose- and time-dependent manner, especially in the antral mucosa. Thus, ammonia chronically administered orally in rats led to changes in gastric mucosal structures and functions. The results suggest that the ammonia produced by HP partly plays an etiologic role in chronic atrophic gastritis.
 ...
PMID:Chronic effect of intragastric ammonia on gastric mucosal structures in rats. 198 2


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>