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)

We have undertaken the analytical fractionation of epithelial cells from toad urinary bladder, a tissue extensively used to study epithelial transport of ions and water. In an attempt to establish markers for the main subcellular organelles, a number of enzymes were assayed in cell homogenates. The nearly ubiquitous plasma membrane marker 5'-nucleotidase, and the transferases that donate N-acetylglucosaminyl, galactosyl, and sialyl residues to glycoproteins and glycolipids in the Golgi complex were not detectable. Glucose-6-phosphatase activity was low in relation to that of nonspecific phosphatases and, therefore, not suitable for identifying the endoplasmic reticulum. Like the cytosolic enzyme lactate, dehydrogenase, catalase was essentially found in the high-speed supernatant, with a noteworthy part of aminopeptidase (substrate, leucyl-beta-naphthylamide) and NAD glycohydrolase. Other enzymes, including cytochrome c oxidase, acid phosphatase, acid N-acetyl-beta-glucosaminidase, alkaline phosphatase, alkaline phosphodiesterase I, nucleoside diphosphatase (substrate ADP), oligomycin-resistant Mg++-ATPase, and mannosyltransferase (acceptor, dolichylphosphate) were fairly active and largely sedimentable. After differential centrifugation, cytochrome oxidase, acid phosphatase, and acid N-acetyl-beta-glucosaminidase were typically associated with the large granule fraction, whereas the other sedimentable enzymes exhibited a broad distribution profile overlapping the nuclear, large granule, and microsome fractions. Their behavior in density equilibrium centrifugation is examined in a companion paper.
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PMID:Subcellular fractionation of epithelial cells from toad urinary bladder. 1. Assay of marker enzymes and differential centrifugation. 250 71

The dose dependent effect of superoxide dismutase in providing protection against oxygen free radicals mediated tissue damage was investigated. Xanthine-xanthine oxidase system was used to generate oxygen free radicals in vitro and damage renal brush border membrane of mice. At lower concentrations, superoxide dismutase was found to rather aggravate renal brush border membrane damage as shown by significant increase (p less than 0.05) in the malondialdehyde levels and corresponding decrease (p less than .05) in the activities of marker enzymes of renal tissue injury i.e. alkaline phosphatase, gamma-glutamyl transpeptidase and leucine aminopeptidase except maltase whose activity increased correspondingly. At higher doses of superoxide dismutase, significant protection (p less than .05) was observed against tissue damage in a dose dependent manner. On the other hand, catalase and mannitol provided dose dependent protection and their combinations with superoxide dismutase could alleviate the enhanced tissue damage produced by lower doses of superoxide dismutase. The implications of these findings have been discussed.
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PMID:Concentration dependent function of superoxide dismutase in oxygen free radicals mediated tissue injury in renal brush border membrane. 281 3

One hundred reference strains and 1,240 clinical isolates representing 26 species of the family Micrococcaceae were used to evaluate the potential of tests for synergistic hemolysis, adherence to glass, pyroglutamyl-beta-naphthylamide hydrolysis, and susceptibility to a set of five antimicrobial agents for differentiating these species and strains within the species. Sixty-eight percent of the clinical isolates exhibited synergistic hemolysis; 69% of the clinical staphylococci but none of the micrococci or stomatococci were adherence positive, and 92% of the strong positive adherence reactions were produced by strains of Staphylococcus epidermidis. Strains from 15 of the species were pyroglutamyl-beta-naphthylamide positive, but this test separated Staphylococcus xylosus from other novobiocin-resistant staphylococci and Staphylococcus intermedius from other coagulase-positive species. A polymyxin B disk helped differentiate S. epidermidis from most other coagulase-negative staphylococci, and a bacitracin disk (10 U) helped differentiate Staphylococcus haemolyticus from most other novobiocin-susceptible staphylococci. All strains that were susceptible to furazolidone and resistant to Taxo A disks (bacitracin, 0.04 U; BBL Microbiology Systems, Cockeysville, Md.) were staphylococci. We observed a 91% correlation between species identification obtained with the Staph-Ident system (Analytab Products, Plainview, N.Y.) and conventional methods; but the micrococci and stomatococci were incorrectly identified as staphylococci with Staph-Ident, and several isolates of S. epidermidis were misidentified as Staphylococcus hominis because they were alkaline phosphatase negative. Both these problems can be prevented by adding the simple tests we describe to those already recommended when the Staph-Ident system is used to identify isolates of gram-positive, catalase-positive cocci.
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PMID:Characteristics of coagulase-negative staphylococci that help differentiate these species and other members of the family Micrococcaceae. 284 32

Subcellular biochemical changes in the jejunal mucosa have been compared in dogs with either aerobic or anaerobic bacterial overgrowth to explore relationships between composition of the flora and mucosal damage. Affected animals comprised 17 German shepherd dogs with chronic diarrhea or weight loss, or both. Analysis of duodenal juice demonstrated aerobic overgrowth in 10 cases, most frequently comprising enterococci and Escherichia coli, and obligate anaerobic overgrowth in 7 cases, most frequently including Clostridia spp. Histologic changes were minimal; however, examination of peroral jejunal biopsy specimens by sucrose density gradient centrifugation revealed specific biochemical abnormalities. In the dogs with aerobic overgrowth, there was a selective loss of brush border alkaline phosphatase activity, and gamma-glutamyl transferase activity was increased, whereas activities of disaccharidases and aminopeptidase N were unaltered. In contrast, anaerobic overgrowth was associated with a reduction in brush border density, indicative of a considerable fall in the glycoprotein-to-lipid ratio of the brush border membrane, whereas brush border enzyme activities were unaltered. There was a loss of peroxisomal catalase activity in dogs with aerobic overgrowth, and an indication of mitochondrial disruption in dogs with anaerobic overgrowth, but little evidence for damage to other subcellular organelles. These findings demonstrate that aerobic and anaerobic overgrowth may be associated with distinct but different mucosal abnormalities particularly affecting the brush border membrane.
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PMID:Comparison of the biochemical changes in the jejunal mucosa of dogs with aerobic and anaerobic bacterial overgrowth. 288 1

Male Wistar rats received a low-protein (4.5% protein) diet during 30 days, and T-2-toxin was administered to them through a gastric tube, in a dose of 0.54 mg/kg, during 15 days. The results obtained showed activation of hepatic lysosomal enzymes (sulfatase A and B aryl and beta-glucosidase) and alkaline phosphatase, and to an essential suppression of enzymatic activity of peroxisomes - catalase, glycolate oxidase and D-amino acid oxidase. A sharp aggravation of the intoxication symptoms and pronounced intensification of changes in enzymatic activity in the liver, spleen, thymus and blood serum were recorded in the animals given T-2 toxin simultaneously with the low-protein diet.
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PMID:[Enzyme parameters in the evaluation of the combined effects of protein deficiency and T-2 mycotoxin]. 289 95

The genetic structure of two Chukot Evens subpopulations (314 individuals) for electrophoretic protein systems and taste sensitivity to PTC was studied. 17 of the 39 loci were polymorphic (43.59%). The following systems were completely monomorphic: diaphorase NAD H (Dia); glucose-6-phosphate dehydrogenase (G-6-PD); glutamatoxalate transaminase (GOT); carbonic anhydrase (Ca-1); catalase (Ct), lactate dehydrogenase (loci LDH-A and LDH-B); leucine aminopeptidase (Lap); malate dehydrogenase (MDH); purine nucleoside phosphorylase (PNP); superoxide phosphorylase (PNP); superoxide dismutase (SOD); phosphoglucomutase-2 (PGM2); cholinesterase (locus E1); red cell esterase (4 loci); albumin (Alb); hemoglobin (Hb A and B); ceruloplasmin (Cp); and blood, gren, using the standard method. The following systems were polymorphic: red cell acid phosphatase (AcP); phosphoglucomutase-1 (PGM1); 6-phosphogluconate dehydrogenase (PGD); glutamatepyruvate transaminase (GPT); glyoxalase-1 (GLO-1); esterase (EsD); adenilatkinase (AK); alkaline phosphatase (Pp); cholinesterase (locus E2); haptoglobin (Hp); transferrin (Tf); group-specific component (Gc) and ABO, MN, Lewis, P blood groups and taste sensitivity to PTC. The following allele frequencies for polymorphic loci have been detected: AKI = 0.994; GLO = 1I = 0.082; GPT1 = 0.653; AcPA = 0.400; AcPB = 0.599; AcPC = 0.001; PGDA = 0.944; PGM1(1) = 0.906; EsD1 = 0.897; E2+ = 0.048; HpI = 0.394; GcI = 0,919; Tfc = 0.987; r(O) = 0.669; p(A) = 0.184; q(B) = 0.146; M = 0.711; Le = 0.411; P1+ = 0.521; t = 0.295. The genetic structure of Chukot Evens population is significantly nearer to that of the other ethnic groups of the North-East, in comparison with the genetic structure of Evenks of the Middle Siberia.
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PMID:[Genetic structure of the populations of native inhabitants in the northeastern USSR. V. The Chukot Evens]. 293 99

As a first step in studies of the molecular mechanism(s) underlying gentamicin toxicity, rat kidney cortex has been subfractionated using differential centrifugation. An analytical, rather than preparative approach was used. DNA was used as a marker for the nuclei, cytochrome oxidase for mitochondria, acid phosphatase for lysosomes, catalase for peroxisomes, NADPH-cytochrome c reductase for the endoplasmic reticulum, p-nitrophenyl-alpha-mannosidase (at pH 5.5) for the Golgi apparatus, AMPase for the plasma membrane in general, and alkaline phosphatase for the brush border, and lactate dehydrogenase for the cytosol. In addition, electron microscopy was performed on the subfractions obtained. The distributions of subcellular markers obtained here for the rat kidney cortex closely resemble the corresponding distributions reported for rat liver. This procedure can now be used to look for biochemical and/or toxic changes which might be reflected in an altered distribution pattern for marker enzymes.
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PMID:Biochemical effects of gentamicin on rat kidney cortex. I. Analytical subfractionation of control tissue. 303 Jul 99

As a first step in studies on the molecular mechanism(s) underlying gentamicin toxicity, the effect of treating rats with this aminoglycoside antibiotic (100 mg/kg once or twice daily for 3 days) on the analytical subfractionation of the kidney cortex has been examined. DNA was used as a marker for the nuclei, cytochrome oxidase for mitochondria, acid phosphatase for lysosomes, catalase for peroxisomes (with reservations; see the companion paper), NADPH-cytochrome c reductase for the endoplasmic reticulum, p-nitrophenyl-alpha-mannosidase (at pH 5.5) for the Golgi apparatus, AMPase for the plasma membrane in general and alkaline phosphatase for the brush border, and lactate dehydrogenase for the cytosol. In addition, the presumptive lysosomal hydrolases N-acetyl-beta-D-glucosaminidase, p-nitrophenyl-alpha-mannosidase (at pH 4.5), cathepsin D, and DNase II were monitored. Electron microscopy was also performed on the subfractions obtained. The only significant biochemical changes brought about by gentamicin treatment were that N-acetyl-beta-D-glucosaminidase demonstrated both a greater total activity and a larger enrichment in the 104,000gav pellet, while p-nitrophenyl-alpha-mannosidase at pH 4.5 demonstrated the same total activity and a greater enrichment in the 104,000gav pellet. Since myeloid bodies were shown by electron microscopy to sediment primarily with the 500gav and 10,000gav pellets, the biochemical changes seen cannot be associated with these morphological structures. These findings suggest that selective changes in a certain subpopulation(s) of lysosomes or in certain lysosomal enzymes may be involved in the early stages of gentamicin toxicity. On the other hand, no lysosomal membrane damage was observed here, since both the latency of acid phosphatase and the recovery of this activity in the soluble cytosol were unchanged. The present investigation may also have relevance for the dosage and duration of gentamicin treatment chosen in clinical situations.
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PMID:Biochemical effects of gentamicin on rat kidney cortex. II. Analytical subfractionation after short-term, high-dose treatment. 303 Aug

Asbestos-associated damage to cells of the respiratory tract in vitro can be prevented by the simultaneous addition of scavengers of active oxygen species to cultures. To determine if administration of scavenger enzymes to animals and humans is a plausible approach to the prevention of asbestos-induced lung disease, osmotic pumps were filled with various concentrations of PEG-coupled catalase and implanted subcutaneously into Fischer 344 rats over a 28-day period. At 3, 14, and 28 days after implantation of the pumps, the animals were evaluated for levels of catalase in serum and lung. In addition, lung tissue and lavage fluids were examined at 28 days for biochemical and morphologic indications of cell injury, inflammation, and fibrotic lung disease. At all time points examined, the administration of PEG-catalase caused a dosage-dependent increase in serum levels of catalase. The levels of lung catalase were evaluated at 28 days but not at earlier time periods. In comparison to control rats, the amounts of enzymes (lactic dehydrogenase, alkaline phosphatase), protein, and cells in lavage fluids from treated animals were unaltered. Moreover, the lungs showed no evidence of inflammation or fibrotic disease as determined by differential cell counts in lavage and measurement of hydroxyproline. These studies suggest that administration of PEG-catalase does not cause injury or other alterations in lung tissue and can be pursued as a feasible approach to prevention of asbestosis.
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PMID:Approaches to prevention of asbestos-induced lung disease using polyethylene glycol (PEG)-conjugated catalase. 303 29

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
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PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56


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