Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intermethod analytical variability of 59 commercially available control sera was compared with that of patient sera. For this purpose, patient and control sera were assayed with respect to ten constituents (albumin, alkaline phosphatase, alpha-amylase, cholesterol, glucose, iron, lactate dehydrogenase, creatinine, protein, and urea), each with two analytical methods. Only 6 of the 59 control materials showed an intermethod analytical variability comparable to that of the patient sera for all of the determinations. The use of patient sera for the calibration of routine analytical methods is recommended.
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PMID:Comparison of intermethod analytical variability of patient sera and commercial quality control sera. 44 52

The activities of several enzymes in urine are masked by the presence of interfering substances in native urine. From several methods proposed for the removal of low molecular mass interferences dilution, dialysis, gel filtration, and ultrafiltration have been successfully applied. Gel filtration seems to be of these most suitable. I is effective, accurate, precise and economical. Scale-down procedures provide for acceptable speed. By this method the complete separation of lactate dehydrogenase, gamma-glutamyltransferase, alkaline phosphatase, arylsulphatase A, alpha-glucosidase, beta-galactosidase, trehalase, N-acetyl-beta-glucosaminidase, beta-glucuronidase and leucine arylamidase from low molecular mass substances, e.g. a heat-stable, competitive inhibitor of N-acetyl-beta-glucosaminidase was possible. The preparation and determination of urinary enzymes should be thoroughly standardized and controlled. Acceptable precision (coefficient of variation less than 10% between-day) can be achieved with manual spectrophotometric methods.
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PMID:Preparation of urine for enzyme determinations by gel filtration. 44 74

The relative sensitivity of urinary enzyme measurements for detecting renal damage was determined for two nephrotoxins. Injection of a single dose of sodium phosphate (10 mmoles/kg) caused damage to the proximal tubules and led to a 15 fold increase in lactate dehydrogenase (LDH) activity excreted into the urine. In contrast to this change the serum LDH remained normal. Similar results were obtained following the injection of cephaloridine (2 g/kg) with an 18 fold increase in urinary LDH and a marginal increase in urinary glutamate dehydrogenase (GDH). By contrast the serum LDH was unchanged. Urinary enzymes are therefore more sensitive for detecting renal injury than enzymes. The four enzymes investigated are located in specific regions of the cell so that the involvement of the organelles and regions of the cell can be followed. Damage to the organelles does not appear to occur as the excretion of the lysosomal enzymes remained normal and only in the case of cephaloridine were marginal changes in the mitochondrial GDH excretion seen. The average alkaline phosphatase was also normal suggesting no gross damage to the plasma membrane although a few individual rats excreted abnormal activities of alkaline phosphatase. These rats however, also excreted high activities of LDH. This suggests that damage to the membrane causes leakage of LDH and in severe cases release of the plasma membrane enzyme alkaline phosphatase. The administration of cephaloridine at various doses showed that urinary enzyme measurements were as sensitive as histology for demonstrating renal damage and that of these enzymes, LDH was by far the most useful.
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PMID:The sensitivity of urinary enzyme measurements for detecting renal injury. 44 87

Male rats were housed singly in metabolic cages, injected i.v. with cephaloridine, 24 h urine samples collected successively; then the rats were killed for obtaining the kidneys of corresponding animals. The concentrations of protein, aminopeptidase (AP), alkaline phosphatase (aPP), lactic dehydrogenase (LDH), and aldolase (ALD) were determined in urine and the percentages of injured proximal tubules counted in sections stained for aPP. The results from individual animals were: (1) After placing animals singly in metabolic cages large but not systematic changes of urinary enzyme concentrations occurred. After 6-10 days the enzymes reached steady state levels. (2) After a single injection of cephaloridine a dose dependent injury of proximal tubules was observed, the urinary LDH content correlating best with the tubular injury (r greater than 0.93) and giving up to 1,000 fold increases above normal values. (3) A circadian rhythm of the susceptibility of rat kidney for cephaloridine was observed, the smallest response was seen when the animals were injected at 7 a.m. and the largest after injection at 7 p.m. (4) In subacute toxicity studies urinary LDH was increased on day 2 above the extent after a single dose, but declined on day 3 to reach normal levels after 8 to 10 days (time of sacrifice). The kidneys revealed practically normal histology. The other enzymes studied had also returned to normal values. This indicates some adaptation mechanism.
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PMID:Relevance of enzyme evaluations in 24h urine to rat kidney injury caused by i.v. cephaloridine injection. 44 88

The diagnostic value of a strikingly elevated serum lactate dehydrogenase (LDH) level in association with only small or no increases in SGOT and alkaline phosphatase levels was noted in five patients with proved renal infarction. Four had renal artery embolism and infarction in association with atrial arrhythmias; one had an acute extension of an abdominal aortic aneurysm occluding the renal artery. Other causes of a considerable isolated increase in the serum LDH level such as hemolysis and myocardial infarction can usually be easily excluded.
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PMID:Elevation of serum lactate dehydrogenase levels in renal infarction. 44 17

Endometrial cells isolated from uteri of ovariectomized rats were treated in vitro with 1 X 10(-9) M estradiol-17 beta (E2beta) to analyze early changes in membrane properties during hormone-induced growth. After 30-min exposure to E2beta at 22 degrees C, cells exhibited an enhanced capacity to bind erythrocytes (hemadsorption) in the presence of concanavalin A (Con A) to 237% of the level in paired controls. Fluorescence microscopy revealted that approximately 25% of cells exposed to E2beta, but not estradiol-17 alpha (E2alpha), showed a redistribution into polar clusters of Con A-binding sites that were dispersed in random patches at the external surfaces of control cells. These hormore-induced membrane alterations were abolished by prior treatment of cells with inhibitors of thiol proteinase activity of the cathepsin B1 (CB1) type, such as leupeptin and iodoacetate. Leupeptin at 4.5 X 10(-7) M also reduced the affinity of [3H]E2beta binding to intact cells but did not influence specific binding of the hormone to macromolecular components of cytosol. A pronounced increase in the availability of endogenous CB1, But not of alkaline phosphatase, succinate, or lactate dehydrogenase, in the extracellular media was elicited within 30 min after E2beta treatment. In cells cultured in chemically defined medium for up to 48 h, E2beta, but not E2alpha, enhanced cell proliferation and stimulated [3H]thymidine incorporation into macromolecular form. These E2beta-induced effects were abolished by prior treatment of cells with liposome-entrapped leupeptin at a final concentration of 7 X 10(-8) M. The net rate of intercellular adhesion among endometrial cells was also enhanced by E2beta. This hormonal response was diminished by prior exposure to leupeptin. Fractionation of cells by selection for adhesiveness due to E2beta exposure for 30 min yielded a subpopulation of rapidly dividing cells which surpassed their less adhesive counterparts in cathepsin secretion and in Con A-mediated hemadsorption. These results indicate that leupeptin-sensitive proteinase activity may contribute to membrane and growth modifications elicited by E2beta treatment in endometrial cells.
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PMID:Estrogen-induced membrane alterations and growth associated with proteinase activity in endometrial cells. 45 77

Mycotoxic porcine nephropathy was induced by p.o. administration of crystalline ochratoxin A for periods of 5 days, 3 months and 2 years. Enzyme activities of the renal tissue were studied histochemically. These were NADH-tetrazolium reductase, NADPH-tetrazolium reductase, lactate dehydrogenase, isocitrate dehydrogenase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, alpha-glycerophosphate dehydrogenase, unspecific acid phosphatase and unspecific alkaline phosphatase. The activity of NADH-tetrazolium reductase and succinate dehydrogenase was reduced in the proximal tubule of all nephrons after 5 days ochratoxin A exposure and remained reduced after 3 months and 2 years exposure. The effect of ochratoxin A on these enzymes would appear to cause the impairment of proximal tubular function and the morphological changes observed in the proximal tubule in ochratoxin A-induced mycotoxic porcine nephropathy. The localization of alterations in enzyme activity corresponds to the localization of ochratoxin A previously demonstrated in the kidney. The activities of NADPH-tetrazolium reductase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and unspecific alkaline phosphatase were reduced focally corresponding to the areas with focal tubular atrophy and the degree of reduction was roughly parallel to the degree of atrophy.
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PMID:Ochratoxin A-induced mycotoxic porcine nephropathy: alterations in enzyme activity in tubular cells. 47 26

The overall performances of several enzyme reagent kits for alkaline phosphatase, creatine kinase, lactic dehydrogenase, and aspartate aminotransferase were evaluated using an ABA-100 Bichromatic Analyzer. Interassay precision using this instrument with commercial reagents compared well with published data for similar analyses performed at university hospitals and referral laboratories. Significantly poorer precision with lower limits of linearity was observed when reagents recommended for use at 30 C were used at 37 C. Significant differences in measured levels of creatine kinase, lactic dehydrogenase, and aspartate aminotransferase due to different lots of expendable cuvettes were found for elevated levels of these enzymes. All kit reagents met manufacturers' claims for stability; however, different absolute levels of lactic dehydrogenase were observed with one kit reagent on successive days. Slight hemolysis affected creatine kinase levels measured with some reagent kits significantly more than others.
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PMID:Evaluation of commercial enzyme reagent kits by use of a semiautomated chemistry analyzer. 47 90

Sets of survey specimens having known linear interralationships were analyzed on four occasions by approximately 450 laboratories for the five enzymes lactate dehydrogenase, aspartate aminotransferase, creatine kinase, alanine aminotransferase, and alkaline phosphatase. The results are summarized in terms of the apparent precision and relative accuracy of various analytical systems, and some apparent problems in enzyme assays are identified. The results show that interlaboratory differences in enzyme analyses are not due primarily to differences in the way laboratorians utilize their analytical systems but rather are due to fundamental differences in the instruments and reagents supplied to the laboratorians. The attainment of interlaboratory comparability of enzyme analyses is a problem that can best be addressed by the manufacturers of instruments and reagents, rather than by individual laboratorians.
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PMID:The 1978 College of American Pathologists survey of analyses of five serum enzymes by 450 laboratories. 47 5

In acute experiment the following results were obtained: the DL50 value after intragastric administration -- 8.2 g/kg of body weight, after intraperitoneal administration -- 1.33 g/kg of body weight. In the studies on acute effect irritating skin and eye of a rabbit -- only a slight inflammatory reaction in conjunctivae was found. Studies on sensitizing effect carried out on guinea pigs did not reveal any symptoms which would give evidence of an alergic effect of the dye. Lima's test did not reveal any cumulative effects of polactine G Yellow, 8-weeks experiment on 30 male rats, administered with 0.5 g/kg and 1.6 g/kg, gave the following results: in the group of rats exposed to 1.6 g/kg an increased excretion of phenol red with urine, lowered activity of aminotranspherases (AspAT and A1AT), increased activity of lactic dehydrogenase and alkaline phosphatase in the blood serum and increased relative liver weight and relative and absolute weight of the kidney. In the group of rats exposed to 0.5 g/kg of polactine yellow G, increased alkaline phosphatase in blood serum and increased relative and absolute liver weight was found. In histopathological studies in acute and subacute experiment, a damage to gastric wall was found. In addition, an increased damage to parenchymatous organs, of reversible degeneration nature, was found.
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PMID:[Evaluation of acute and subacute toxic effects of polactine yellow G]. 48 Nov 97


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