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:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In the course of the present investigation, three chelating agents (2,3,2 tet, cyclam or EDTA) were tested for their therapeutic effect on nickel and cobalt poisoned toad. 2. Our results showed that EDTA appears to be superior to the two other ligands, which have been proved to be chemical ligands for Ni and Co in vitro. 3. EDTA was able to prevent disturbances in the activities of serum aspartate and alanine aminotransferases, alkaline phosphatase, total protein, urea, uric acid and blood glucose level. 4. Our results suggest caution in the use of 2,3,2 tet or cyclam in human Ni and Co intoxication.
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PMID:Therapeutic effectiveness of 2,3,2 tet, cyclam and EDTA in toads exposed to lethal doses of nickel and cobalt. 197 57

NADH oxidase activity has been detected at the ultrastructural level using cerium ions to trap H2O2 generated by the enzyme (via intermediate reactive oxygen species). In an attempt to localize NADH oxidase activity at the light microscope level using the cerium-diaminobenzidine (DAB)-nickel-H2O2, the cerium-DAB-cobalt-H2O2 or the cerium-alkaline lead procedures, the distribution patterns of the revealed enzyme were found to be identical to those for non-specific alkaline phosphatase and especially 5'-nucleotidase activity. With the cerium-DAB-cobalt-H2O2 visualization procedure, the distribution pattern of the final reaction product was similar to that obtained with the other two techniques but much less final reaction product was formed. Incubations for NADH oxidase activity performed in the presence of exogenous catalase or in the absence of catalase or peroxidase inhibitors did not affect the staining intensity, whereas inhibitors of 5'-nucleotidase (EDTA) and non-specific alkaline phosphatase (levamisole) always did. Therefore, phosphatases contribute to the formation of the final reaction product. Since NADH initially cannot be hydrolysed by either of these two phosphatases, then presumably nucleotide pyrophosphatase (E.C.3.6.1.9) cleaves NADH into 5'-AMP and nicotinamide mononucleotide in a first step. Both nucleotides can be hydrolysed further by the two monophosphatases. These then generate cerium phosphate which is detected by the DAB-nickel-H2O2, DAB-cobalt-H2O2 or lead visualization methods.
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PMID:Pitfalls in the light microscopical detection of NADH oxidase. 236 89

Various chromogen protocols for visualizing peroxidase and alkaline phosphatase activity in immunoenzyme histochemistry were compared with respect to their sensitivity. They were tested on tissue sections of human skeletal muscle and in an antigen spot test using antibodies against slow skeletal muscle myosin. The chromogens included 3-amino-9-ethylcarbazole (AEC), 3, 3'-diaminobenzidine (DAB), p-phenylenediamine-pyrocatechol (PPD-PC) and 4-chloro-1-naphthol (CN) in peroxidase histochemistry, and 5-bromo-4-chloro-3-indolyl phosphate-nitro blue tetrazolium salt (BCIP-NBT), BCIP-tetra nitro blue tetrazolium salt (TNBT) and various combinations of substituted naphthol phosphate-diazonium salt in alkaline phosphatase histochemistry. DAB, CN, and PPD-PC were also employed with imidazole and DAB in addition to Co2+ and Ni2+ ions. The results indicate that DAB-imidazole and DAB-Co2+ and Ni2+ ions are the most sensitive chromogen protocols for visualizing peroxidase activity. Although no large differences were found between the various chromogen protocols for visualizing alkaline phosphatase activity, the protocol BCIP-TNBT is especially recommended. Furthermore, the various chromogen protocols were evaluated as to stability of chromogen solutions and final precipitates, background staining, localization properties, and enhancement of enzyme activity.
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PMID:Sensitivity of various visualization methods for peroxidase and alkaline phosphatase activity in immunoenzyme histochemistry. 241 13

By the neuroanatomical tracing technique based on uptake, transport, and immunocytochemical detection of injected Phaseolus vulgaris leucoagglutinin (PHA-L), fiber trajectories of labeled neurons can be followed with great accuracy to their termination areas. To further analyze the connectivity of these fibers, the target neurons must be chemically characterized. In vibratome and frozen sections of rat brain, we tried to visualize PHA-L-labeled fibers and, simultaneously, the target neuron-related antigen. As a model system we used the projection from the pre-frontal cortex to histaminergic neurons in the posterior hypothalamic region. We tested "sequential" and "pooled" immunocytochemical procedures. In the sequential procedure, the two antigens are detected by two successive and complete immunocytochemical staining procedures, with primary antibodies raised in different animal species and with different chromogens for the final visualization. In the pooled procedure, the sections are incubated with mixtures of primary and secondary antibodies, after which the procedure is similar to the sequential procedure. We obtained excellent results on vibratome sections with a sequential procedure using first conventional peroxidase immunocytochemistry (goat anti-PHA-L primary antibody) to visualize the transported PHA-L (brown reaction product), and subsequently alkaline phosphatase immunocytochemistry (rabbit anti-histidine decarboxylase primary antibody) to locate the histaminergic neurons (blue reaction product). The resulting preparations deteriorate, however, after 1-2 months of storage. Good results were also obtained with a double peroxidase procedure on frozen sections, using nickel-enhanced diaminobenzidine to visualize the PHA-L (dark blue reaction product), and diaminobenzidine (brown reaction product) to visualize the second antigen. The quality of these preparations is permanent.
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PMID:Double-label immunocytochemistry: combination of anterograde neuroanatomical tracing with Phaseolus vulgaris leucoagglutinin and enzyme immunocytochemistry of target neurons. 243 83

In order to determine the specific action of cadmium on bone metabolism, the effect of cadmium on alkaline phosphatase activity, a marker enzyme of osteoblasts, was compared with that of other divalent heavy metal ions, i.e., zinc, manganese, lead, copper, nickel and mercury (10 microM each), using cloned osteoblast-like cells, MC3T3-E1. Cadmium had the strongest inhibitory effect on alkaline phosphatase activity of the cells among the metals tested. At the same dose, however, cadmium failed to inhibit cellular glucose-6-phosphatase and lactate dehydrogenase activities, suggesting that the inhibitory effect of cadmium on alkaline phosphatase was specific and was not dependent on cell injury. Cadmium treatment caused a significant decrease in cellular zinc level, but mercury treatment had no such effect at the dose inhibiting alkaline phosphatase activity. There was a good correlation between decrease of cellular zinc level and inhibition of alkaline phosphatase activity in cadmium-treated cells. Concomitant treatment of the cells with zinc prevented the cadmium-induced inhibition of alkaline phosphatase activity. However, this was not the case in the mercury-induced inhibition. Cadmium also inhibited the mineralization of osteoblasts. When 10 or 20 microM zinc was concomitantly added to the cultures, the inhibition of mineralization was prevented. These data suggest that the inhibitory effect of cadmium in osteoblasts may be closely related to its influence on the cellular zinc metabolism.
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PMID:Preventive effects of zinc on cadmium-induced inhibition of alkaline phosphatase activity and mineralization activity in osteoblast-like cells, MC3T3-E1. 274 54

New light microscopic visualization methods were developed for the histochemical detection of non-specific alkaline and acid phosphatase, Mg-, Ca- and Na, K-dependent adenosine triphosphatase, myosin adenosine triphosphatase, glucose-6-phosphatase, 5'-nucleotidase and thiamine pyrophosphatase with cerium ions as trapping agents in cryostat and plastic sections. The techniques are based on the conversion of cerium phosphate into cerium perhydroxide by H2O2 which decomposes at 55 degrees-60 degrees C into cerium hydroxide and oxygen radicals. These radicals are able to oxidize diaminobenzidine (DAB) to DAB brown. Addition of nickel ions to the DAB-H2O2 mixture generates bluish-black stained nickel-DAB complexes. Compared with the classical metal precipitation, azo, azoindoxyl and tetrazolium procedures the H2O2-DAB and especially the H2O2-DAB-nickel methods provided identical or superior results in catalytic phosphatase histochemistry and immunohistochemistry when using non-specific alkaline phosphatase as the enzyme label.
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PMID:The cerium perhydroxide-diaminobenzidine (Ce-H2O2-DAB) procedure. New methods for light microscopic phosphatase histochemistry and immunohistochemistry. 285 63

Enhanced lipid peroxidation was observed in livers of rats killed 24 hr after sc injection of nickel chloride (NiCl2) (750 mumol per kg), as evidenced by 13-fold increase of conjugated dienes in microsomal lipids and 4-fold increase of thiobarbituric acid (TBA) chromogens in hepatic cytosol. Histologic examination of livers from rats killed one to three days after NiCl2 injection (500 mumol per kg) showed microvesicular fatty metamorphosis, mild hydropic degeneration, and foci of inflammation. Microvesicular steatosis of hepatocytes was confirmed by electron microscopy. Dose-related increases of serum aspartate aminotransferase (ALT) activity (up to 7-fold vs controls) and alanine aminotransferase (ALT) activity (up to 3-fold vs controls) were observed 24 hr after injection of NiCl2 (125 to 750 mumol per kg); diminished serum alkaline phosphatase activity (up to 72 percent reduction vs controls) was seen at NiCl2 dosages from 375 to 750 mumol per kg. Diethyldithiocarbamate did not influence the effects of NiCl2 on TBA-chromogens in liver homogenates or on serum AST and ALT activities but acted synergistically with NiCl2 to diminish serum alkaline phosphatase activity and to increase serum bilirubin concentration. This study demonstrates that parenteral administration of NiCl2 to rats produces acute hepatic toxicity, with enhanced lipid peroxidation, microvesicular steatosis, and increased serum AST and ALT activities.
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PMID:Hepatic toxicity of nickel chloride in rats. 300 32

Guinea pig skin was treated with 50 mg/kg sodium lauryl sulphate (SLS) and nickel (Ni) alone and in combination (50 mg/kg SLS and 50 mg/kg Ni) for 7 and 14 days. Release of acid phosphatase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, beta-glucuronidase, lactic dehydrogenase and malic dehydrogenase was observed, following treatment with SLS and Ni alone or in combination. Similarly, the skin contents of amino nitrogen and sulphydryl groups also increased significantly. These alterations were slightly more marked when the skin was treated simultaneously with the combination of SLS and Ni. The present study suggests that industrial workers or populations exposed simultaneously to SLS and Ni are more prone to dermal irritation or inflammation.
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PMID:Effect of sodium lauryl sulphate and nickel alone and in combination on the skin of guinea pigs. 317 54

The effect of essential trace metals on bone metabolism was investigated in the femoral diaphysis of weanling rats. Oral administration of zinc (1.53-306 mumol/100 g body weight) for 3 days produced significant increases in alkaline phosphatase activity and DNA content. These biochemical indices were also increased by oral administration of chromium (III), cobalt, copper, manganese, and nickel with the dose of 1.53 mumol/100 g. With the dose of 15.3 mumol/100 g of above all metals, except zinc, the enzyme activity was significantly decreased in comparison with control, while DNA content was not decreased significantly. Moreover, the effect of zinc on alkaline phosphatase activity and DNA content was not enhanced by simultaneous administration of other metals (1.53 mumol/100 g). The present study indicates that, of the essential trace metals, zinc can effectively stimulate the bone growth and calcification with comparatively higher dose levels. This suggests a nutritional significance of zinc on bone growth.
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PMID:Effect of essential trace metals on bone metabolism in weanling rats: comparison with zinc and other metals' actions. 379 21

The effects of zinc on the enzymes of femoral tissue were investigated in weanling rats that had been given zinc sulfate (1.0 mg Zn2+/100 g body wt) p.o. for 3 days. Administration of zinc caused a marked elevation of alkaline phosphatase and acid phosphatase activities, whereas it did not cause significant changes in succinate dehydrogenase, 5'-nucleotidase, ATPase, pyrophosphatase and beta-N-acetylglucosaminidase activities. The effect of zinc was greater on alkaline phosphatase of the femoral diaphysis. Zinc content of the femoral diaphysis was raised significantly by administration of zinc. The addition of zinc in concentrations of 10(-2)-10(2) microM did not produce a significant increase in alkaline phosphatase activity in the femoral diaphysis, indicating that zinc could not activate the enzyme. Administration of cycloheximide or actinomycin D completely inhibited the increase in alkaline phosphatase activity produced by administration of zinc. DNA content of the femoral diaphysis, but not epiphysis, was increased markedly by administration of zinc. The increases in both alkaline phosphatase activity and DNA content of the femoral diaphysis were not caused by administration of copper, manganese, cobalt, nickel and chromium(III). The present investigation suggests that zinc may induce the increase in alkaline phosphatase related to DNA synthesis and, as a result, stimulate bone growth.
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PMID:Action of zinc on bone metabolism in rats. Increases in alkaline phosphatase activity and DNA content. 395 86


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