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)

Vitamin D3 in rachitic chicks stimulates calcium absorption and induces the synthesis of two pools of intestinal calcium-binding protein (CaBP), one soluble and the other membrane bound. Cortisol acetate caused a decrease in calcium absorption which was accompanied by a decrease in soluble CaBP. Cortisol was similarly effective in 1,25-dihydroxyvitamin D3-dosed chicks, suggesting that the glucocorticoid effect was not entirely due to the defective synthesis of this metabolite. Ca absorption was directly correlated with soluble CaBP and alkaline phosphatase and inversely related to the ratio of bound to soluble CaBP. It was further observed that the slope of the Ca absorption vs. soluble CaBP regression line was greater in chicks given 1,25-dihyroxyvitamin D3 compared to those given vitamin D3, and this is interpreted to mean that another factor or condition, in addition to assayed concentrations of soluble CaBP, determines the degree of calcium absorption.
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PMID:Intestinal calcium-binding protein and calcium absorption in cortisol-treated chicks: effects of vitamin D3 and 1,25-dihydroxyvitamin D3. 22 Nov 83

Cortisol 21-amine (21-amino-11beta,17-dihydroxy-4-pregnene-3,20-dione) was prepared and an enzyme immunoassay for cortisol in serum was established using cortisol 21-amine conjugated with alkaline phosphatase. The minimal amount of cortisol detected was 1ng/tube and the measurable range was from 1 to 80 microgram/d1, using 10 mu 1 of serum sample. This enzyme immunoassay satisfied the standard criteria of dilution, accuracy and precision. The values correlated well with those obtained by radioimmunoassay. This enzyme immunoassay is applicable to the routine determination of serum cortisol in any clinical laboratory. Cortisol 21-amine was found to be a useful derivative for preparing cortisol-enzyme conjugate in enzyme immunoassay.
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PMID:Enzyme immunoassay for cortisol in serum using cortisol 21-amine. 36 Apr 90

Cortisol partially prevents the harmful effect of gluten on the jejunal mucosa of patients with gluten-sensitive enteropathy. To investigate further the pathogenesis of this disorder, we analyzed the effect of cortisol in cultures of jejunal specimens obtained by biopsy. Cultures were done with and without gluten or cortisol. Morphology and alkaline phosphatase activity were assessed before and after 24 hours. Biopsies from untreated patients cultured with gluten showed low enzyme values and cuboidal epithelial cells before and after culture. Biopsies cultured in a gluten-free medium showed a threefold increase in enzyme values (P less than 0.01) and morphologic improvement with change to columnar epithelial cells. Cultures with gluten plus cortisol showed rises in alkaline phosphatase and morphologic improvement indistinguishable from cultures without gluten. Cortisol and gluten had no effect on cultures from appropriate controls. Cortisol thus prevents the harmful effects of gluten on biopsies from patients with gluten-sensitive enteropathy in vitro.
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PMID:Gluten-sensitive enteropathy. Inhibition by cortisol of the effect of gluten protein in vitro. 127 29

This paper describes a fully automated assay on the Serono SR1 for the measurement of cortisol in serum, heparinised plasma and urine. The assay incorporates a specific polyclonal antibody to cortisol and cortisol conjugated to alkaline phosphatase as a label. Following immunoincubation, bound and free labelled cortisol are separated by magnetic sedimentation of the antibody complex. Phenolphthalein is liberated by the enzymatic hydrolysis of the substrate (phenolphthalein monophosphate) and the absorbance generated is measured as the assay end-point. All processing steps are performed by the SR1. The assay has good analytical performance with respect to precision (within and between run CVs less than 10 and 11.5% respectively), detection limit (less than 5 nmol/l) and recovery of added cortisol (100 +/- 10%). The assay agrees well with cortisol concentrations determined by ID-MS and by established immunoassays (r > 0.96). Reference ranges of normal urine samples (pretreated by solvent extraction) are in good agreement with accepted values. The study demonstrates that the SR1 Cortisol assay on the SR1 analyzer is suitable for the routine determination of cortisol in serum, heparinised plasma and urine samples.
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PMID:A fully automated enzyme immunoassay for the measurement of cortisol in biological fluids. 145 15

Cortisol 3-(o-carboxymethyl)oxime (C3-CMO) and a commercially available biotin-hydrazide derivative were used to synthesize a C3-CMO-biotin conjugate. C3-CMO was converted into a N-hydroxysuccinimide ester derivative which in a second reaction step was allowed to interact with the hydrazide derivative of biotin. This simple-to-perform synthesis yielded a conjugate suitable for use as a tracer in immunoassays for cortisol measurement. Employing biotin as the primary probe in a competitive solid phase immunoassay allows for variable end point determination by means of commercially available labeled avidin or streptavidin derivatives. Streptavidin-Europium was used in conjunction with the DELFIA-system for time-resolved fluorometric end point measurement (TR-FIA) throughout the study. In addition, colorimetric end point determination (ELISA) using streptavidin-alkaline phosphatase as a secondary probe was established and evaluated. Both forms of this non-isotopic assay showed excellent correlation with a commercially available radioimmunoassay adapted for salivary cortisol measurement. The lower detection limit was 0.43 nM for a 50 microliters salivary sample. The intra-assay coefficient of variation was 6.7, 4.7 and 4.0% at cortisol concentrations of 2.2, 5.5 and 13.2 nM, respectively (n = 37), and the corresponding inter-assay coefficients of variation were 9.0, 8.6 and 7.1% (n = 50). The competitive immunoassay requires 1.5 h incubation time and shows robust and reproducible performance. The C3-CMO-biotin conjugate allows for sensitive and flexible end point determination of salivary cortisol levels in immunoassays.
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PMID:Synthesis of a cortisol-biotin conjugate and evaluation as a tracer in an immunoassay for salivary cortisol measurement. 147 60

The serum hormone (T3, FT3, T4, FT4, TSH, hTG, a-hTG, GH, PTH, PRL, Cortisol) concentrations, the inorganic phosphate complexes (HPO2-4, H2PO-4, NaHPO-4, KHPO-4, CaHPO4, MgHPO4) and the enzyme activities (Amylase, Lipase, AP, ACE, GOT, GPT, psi-ChE, CK, gamma-GT, LDH) were investigated in 13 haemodialysed children, 7 kidney-transplanted children and in 15 healthy controls. This study confirmed that the kidney plays an important role in the metabolism of hormones. Prior to kidney transplantation 8 of the 11 tested hormone levels of haemodialysed children significantly differed from those of healthy controls, however, after kidney transplantation only two parameters did. The effect of dialysis is the least on the CaHPO4 complex among the different inorganic phosphate complexes. This may play a role in vascular calcification in chronic renal failure patients. The amylase and lipase activity were elevated in haemodialysed group, while in kidney-transplanted children the angiotensin converting enzyme (ACE) and alkaline phosphatase (AP) differed from those of the control group.
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PMID:The serum hormone levels, phosphate complex concentrations and enzyme activities in haemodialysed and kidney-transplanted children. 169 May 69

The lipocortins are a family of calcium-dependent phospholipid-binding proteins that are induced by glucocorticoids and inhibit phospholipase-A2 activity. To determine whether the lipocortins affect the release of PRL from human decidua, decidual cells from term pregnancies were exposed to recombinant lipocortin-I for 96 h, with medium changes at 24-h intervals. Lipocortin-I (0.01-100 nM) caused a time- and dose-dependent inhibition of PRL release, with a half-maximal effective dose of 50 nM. PRL release was inhibited by 27%, 62%, 93%, and 98% at 24, 48, 72, and 96 h, respectively. The cells exposed to lipocortin-I did not release the enzymes alkaline phosphatase and lactic dehydrogenase, indicating that the inhibitory effect on PRL release was not due to cell death. In addition to inhibiting basal PRL release, lipocortin also completely inhibited the stimulation of PRL release by decidual PRL-releasing factor, a 23.5-kDa protein recently purified from human placenta that stimulates the synthesis and release of decidual, but not pituitary, PRL. Hydrocortisone and dexamethasone (0.1-10 microM) had no effect on PRL release, and arachidonic acid (2-100 microM) inhibited rather than stimulated PRL release. Western blot analysis demonstrated the presence of lipocortin-I in decidual cells and conditioned media. On Northern blot, decidual mRNA hybridized to an oligonucleotide for lipocortin-I. These results strongly suggest that lipocortin-I has an autocrine/paracrine role in regulation of the synthesis and release of PRL from human decidual cells.
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PMID:Lipocortin-I inhibits the synthesis and release of prolactin from human decidual cells: evidence for autocrine/paracrine regulation by lipocortin-I. 182 32

Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype.
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PMID:Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells. 217 56

A single intravenous injection of 0.1 mg/g of zymosan led to the formation of granuloma-type clusters of mononuclears in the liver of CBA mice or (CBA X C57B1)F1 hybrid mice. The area occupied by the granulomas grows for 3 to 9 days and then gradually diminishes so that the granulomas disappear practically in one month. Hydrocortisone injected in a dose of 125 mg/kg 2 and 24 hours before or 2 and 24 hours after zymosan inhibited the initiation of granulomas but, at the same time, led to their slower involution. Mice with zymosan-induced granulomas became hypersensitive to the derivate of an endotoxin--prodigiosin, a polysaccharide obtained from S. marcescens. After intravenous infusion of a preparation of corpuscular alkaline phosphatase (CAP) granuloma-like structures also appear in the liver of rats. In distinction from zymosan-induced granulomas they persist for a much longer time (up to 27 weeks). The first signs of CAP-induced granulomas appear in 3 days. The liver per cent by volume occupied by the granulomas gradually doubles by the 15th week and then reduces. At the same time, the number of granulomas per 1 mm3 of hepatic tissue remains practically constant for 3 to 21 weeks from the moment of the induction by CAP. Their average size grows slowly and reaches maximum by the 15th week, with significant variations. Desmine and reticular fibres accumulate in the granulomas, which is evidence of active involvement of hepatic fat-accumulating cells in their formation. The results show that resident macrophages are the triggers of granulomatous inflammation of the liver.
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PMID:[Induction of granulomatous liver inflammation by noninfectious particles]. 229 64

The effects of glucocorticoids (hydrocortisone, dexamethasone) and insulin on enzymatic activities of the intestinal brush border membrane were investigated in an anuran amphibian, Alytes obstetricians, before and during experimental metamorphosis produced by immersion into a thyroxine solution. During experimental metamorphosis, a new epithelium (secondary epithelium) replaces the degenerating primary epithelium. The enzymes studied were three glucidases (maltase, glucoamylase, trehalase) and alkaline phosphatase. In tadpoles reaching the end of premetamorphosis, hormones were injected every day (hydrocortisone, dexamethasone: 25 micrograms/g body wt/day; insulin: 5 mU/g body wt/day, for 3 and occasionally 6 consecutive days. Under such conditions, most of the activities in the primary epithelium increased or remained stable. In animals which completed experimental metamorphosis, the secondary epithelium formed. Hydrocortisone (25 micrograms/g body wt/day) and insulin (5 mU/g body wt/day) treatments significantly decreased the enzymatic activities of the new brush border membrane in animals which received one hydrocortisone and/or insulin injection per day, during 3 consecutive days. Such results, which previously had not been obtained systematically in spontaneously metamorphosing tadpoles (El Maraghi-Ater, Mesnard, and Hourdry (1986). Gen. Comp. Endocrinol. 61, 53-63), emphasize the relative independence of the intestinal metabolism during experimental and spontaneous metamorphosis.
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PMID:Hormonal control of the intestinal brush border enzyme activities in developing anuran amphibians. II. Effects of glucocorticoids and insulin during experimental metamorphosis. 310 33


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