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)

Parathyroid hormone (PTH) has been proposed as a skeletal activator for cyclical protocols of treatment for osteoporosis; among several potential drugs that might serve to depress the subsequent phase of osteoclastic bone resorption, calcitonin is the most selective. Twenty patients aged 50-78 years were enrolled in a study of their biochemical responses during a 14-day activation cycle with synthetic hPTH 1-38, given as a subcutaneous injection of 400 IU/day; half the patients were randomly allocated to receive a subsequent 56-day depressor cycle with calcitonin in a dose of 100 U/day, while the remainder received no further treatment. All patients received an initial 24-h intravenous infusion of hPTH 1-38 (0.5 U/kg/h) to evaluate the PTH-dependent renal synthesis of 1,25(OH)2D. Serum calcium increased from 2.20 +/- 0.07 mmol/l to 2.56 +/- 0.16 (P less than 0.005) during PTH infusion, but was not significantly different from baseline during intermittent treatment. Baseline concentrations of serum 1,25(OH)2D were 22.8 +/- 8.2 pg/ml, increased to 52.2 +/- 25.1 (P less than 0.005) during infusion and remained significantly higher than baseline after 14 days intermittent therapy (33.1 +/- 19.4, P less than 0.05). Gastrointestinal absorption of 45Ca, as represented by alpha (peak fractional absorption/h), increased from 0.397 +/- 0.173 to 0.552 +/- 0.210 (P less than 0.01) during hPTH 1-38 therapy and was moderately correlated with the increment in serum 1,25(OH)2D levels (r = 0.5, P less than 0.03). Daily calcium excretion was significantly increased above baseline during hPTH 1-38 therapy, but there were no correlations between changes in urinary calcium, alpha or serum 1,25(OH)2D levels. Baseline fasting urinary excretion of OH-proline increased during hPTH 1-38 treatment from 30.5 +/- 13.9 mol/mmol creatinine to 43.4 +/- 17.5 immediately after hPTH 1-38 infusion (P less than 0.025), and mean excretion was persistently higher than baseline during intermittent treatment; the increased urine calcium and OH-proline excretion are consistent with PTH-induced activation of bone resorption. Serum alkaline phosphatase and osteocalcin levels increased significantly during a 90-day period of observation after the hPTH 1-38 cycle, which is consistent with increased osteoblast activity in association with coupled bone formation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical responses to sequential human parathyroid hormone (1-38) and calcitonin in osteoporotic patients. 216 92

Inadequate vitamin D intake is an important cofactor in clinical and experimental bone disease induced by chronic cadmium exposure. The interaction was investigated by culture of rat osteoblastic osteosarcoma cells (ROS 17/2.8) in a serum-free medium with equimolar concentrations of cadmium chloride and 1 alpha,25-(OH)2 vitamin D3. After addition of cadmium alone to culture medium, the unstimulated secretion of osteocalcin and cellular alkaline phosphatase activity were inhibited at 10 pM, and of DNA synthesis and proline incorporation into collagen at 500 nM. In the presence of equimolar amounts of cadmium and 1 alpha,25-(OH)2 vitamin D3, all four responses paralleled those of 1 alpha,25-(OH)2 vitamin D3 alone up to the inhibitory concentration of 500 nM cadmium. Neither 10 nM 1 alpha,25-(OH)2 vitamin D3 nor 1 microM cadmium induced synthesis of metallothionein in these cells indicating that the protective effect of D3 was not related to the induction of a metallothionein-like protein in ROS 17/2.8 cells. In the presence or absence of D3, cadmium inhibited osteoblastic function at concentrations below the whole-organ concentration of cadmium in bone as reported in experimental and clinical cadmium-induced osteotoxicity. The extreme sensitivity of ROS 17/2.8 cells to cadmium may relate to the absence of metallothionein synthesis.
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PMID:Toxicity of cadmium to rat osteosarcoma cells (ROS 17/2.8): protective effect of 1 alpha,25-dihydroxyvitamin D3. 231 24

We examined the cytoprotective action of individual amino acids in isolated perfused kidneys during perfusion with either 10 mM lactate or 5 mM glucose. In the absence of amino acids inulin clearance fell rapidly, whereas fractional excretion of phosphate, lactate, or glucose increased to more than 30%; lactate dehydrogenase was released into perfusate and alkaline phosphatase into the urine. Functional deterioration was less in kidneys from rats rendered chronically water diuretic by drinking 5% glucose. Adding 5 mM glycine, L-alanine, beta-alanine, or D-alanine to the perfusate also prevented functional deterioration and release of enzymes. Glycine perfusion increased total phospholipid per microgram DNA by 6%. Aspartate, glutamate, glutamine, taurine, isoleucine, leucine, and valine were not protective. Serine, proline, and alpha-aminoisobutyric acid had small protective effects. Micropuncture measurements of proximal tubular free- and stop-flow pressures showed no effect of L-alanine on glomerular hemodynamics. L-Alanine increased oxygen consumption by both glucose- and lactate-perfused kidneys and increased gluconeogenesis by lactate-perfused kidneys but did not alter renal ATP content or energy charge. L-Alanine was not consumed during 70 min of perfusion and its protective action was not inhibited by blocking transamination with 0.5 mM amino-oxyacetate. The protective action of glycine was not inhibited by blocking glycine metabolism with 0.1 mM cysteamine. Thus the beneficial effects of L-alanine and glycine do not require their metabolism. These observations suggest that small neutral amino acids prevent tubular disruption through their physicochemical effects, which can stabilize membrane protein tertiary structure.
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PMID:Mechanisms of perfused kidney cytoprotection by alanine and glycine. 237 94

Amino acid sequencing of a CNBr digest of the tau protein isolated from bovine brain revealed an amino acid sequence of 17 residues, Pro-Gly-Leu-Lys-Glu-Ser-Pro-Leu-Gln-Ile-Gly-Ala-Ala-Pro-Gly-Leu-Lys, which we call peptide I, with heterogeneity at position 11 of glycine (peptide Ia) and proline (peptide Ib); peptide I showed no homology with the previously reported cDNA-derived mouse and human tau sequences. Antisera raised to synthetic peptides corresponding to peptides Ia and Ib labeled all the bovine tau polypeptides recognized by other monoclonal and polyclonal antibodies to bovine tau. Antisera to peptide Ib did not label any mouse tau polypeptides; however, an anti-Ia antiserum labeled two of the four mouse tau polypeptides. Antisera to both peptides labeled paired helical filaments (PHF) as neurofibrillary tangles, plaque neurites, and neuropil threads in Alzheimer disease brain and PHF polypeptides on immunoblots. Immunostaining with anti-Ia antisera of PHF in tissue sections and PHF polypeptides, but not bovine tau, on immunoblots was markedly increased when pretreated with alkaline phosphatase. These studies suggest that (i) the amino acid sequences of some isoforms of tau peptide might be different from that predicted from cDNAs, (ii) a tau peptide that is absent in the predicted sequences is present in PHF in Alzheimer disease, and (iii) tau in PHF is abnormally phosphorylated.
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PMID:Identification and localization of a tau peptide to paired helical filaments of Alzheimer disease. 250 95

A 12-month prospective controlled study was conducted in 28 patients with acute osteoporotic spine fractures to evaluate and compare the effect of calcitonin treatment and cyclical hormone replacement therapy on forearm bone mineral content (BMC) and bone turnover. We established two treatment groups and a control group of women with postmenopausal osteoporosis (n = 28). Group A (n = 10) received 100 U of calcitonin by subcutaneous self-application on alternate days and oral calcium (Ca) for 6-8 weeks. Group B (n = 10) received cyclical estrogen/gestagen replacement therapy over 12 months and oral calcium. The control group (n = 8) received analgetic treatment and 500 mg Ca daily. BMC was measured by single photon absorptiometry (SPA) with I 125 before and 6 and 12 months after the onset of the therapies. Ca, phosphorus (P), alkaline phosphatase, and 2-hour urinary OH-proline excretion were measured to classify bone turnover. One year after the onset of the two therapies, forearm BMC measured by SPA showed a significant increase in the group under hormone replacement therapy (P less than 0.025) as well as in the calcitonin group (P less than 0.05), although the latter underwent treatment only over a short period (6-8 weeks). In the same period, BMC decreased significantly in the control group (P less than 0.025). These results demonstrate that short-term calcitonin treatment over 6-8 weeks is as effective as long-term hormone replacement therapy, both therapies increasing forearm BMC measured by SPA.
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PMID:Estimated long-term effect of calcitonin treatment in acute osteoporotic spine fractures. 250 7

Previous in vitro studies have shown that salmon calcitonin had direct effects to increase parameters associated with embryonic chicken bone formation and to increase mouse and chicken osteoblast-line cell proliferation. The current studies demonstrate increased cell proliferation (i.e., [3H]-thymidine incorporation into DNA and tetrazolium salt reduction/deposition) in the osteoblastic murine cell line MC-3T3-E1 in response to salmon calcitonin (P less than 0.005) and to human calcitonin (P less than 0.005), but not to human calcitonin gene-related peptide. The current studies also show that salmon calcitonin increased several indices of murine bone formation. We found that 72 hours of exposure to salmon calcitonin [at 5 mU/ml-about 0.37 nM; mU/ml = milliunits of calcitonin activity/ml incubation medium (at 4,000 U/mg protein)] increased net 45Ca deposition (121% of control, P less than 0.05), net [3H]-proline incorporation 149% of control, P less than 0.001), and alkaline phosphatase activity (146% of control, P less than 0.01), in neonatal mouse half-calvaria. The calcitonin-dependent increase in alkaline phosphatase activity was not affected by co-incubation with 1 nM parathyroid hormone. Co-incubation with fluoride (which also increased net [3H]-proline incorporation and alkaline phosphatase activity in neonatal mouse half-calvaria, P less than 0.05, for each) enhanced the osteogenic response to low-dose calcitonin, (i.e., co-incubation with fluoride shifted the biphasic calcitonin dose-response curve to a range of lower calcitonin concentrations). The calcitonin-fluoride combinations had proportional effects on net [3H]-proline incorporation and alkaline phosphatase in the treated mouse calvaria (r = 0.78, P less than 0.005).
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PMID:Calcitonin (but not calcitonin gene-related peptide) increases mouse bone cell proliferation in a dose-dependent manner, and increases mouse bone formation, alone and in combination with fluoride. 250 8

Marrow stroma has been shown to have osteogenic potential. Here we report the characterization of a unique stromal cell line derived from mouse bone marrow (MBA-15), which expresses osteoblastic phenotype in vitro and forms bone in vivo. More than 70% of cells in culture were histochemically positive for alkaline phosphatase. The enzyme levels were enhanced threefold when cultures were treated with dexamethasone. Gel electrophoresis of [3H]-proline-labeled cultures showed that MBA-15 cells produced only type I collagen. These cells were responsive to PTH, as indicated by a 50-fold increase in intracellular cAMP. Prostaglandin E2, but not calcitonin, stimulated cAMP up to 70-fold. When cultures were grown to confluence and fed daily with ascorbic acid and beta-glycerophosphate, the cells formed a Von Kossa positive, thick extracellular matrix, shown to contain hydroxyapatite crystals. MBA-15 cells produced mineralized bone when implanted in diffusion chambers. These results indicate that the MBA-15 cell line possesses osteoblastic features in vitro and osteogenic capacity in vivo.
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PMID:Bone marrow-derived stromal cell line expressing osteoblastic phenotype in vitro and osteogenic capacity in vivo. 254 12

Male Sprague-Dawley rats were challenged with various hyperoxaluric agents including ammonium oxalate, hydroxy-L-proline, and ethylene glycol. All treatments resulted in increased urinary oxalate. Associated with hyperoxaluria was an increase in urinary levels of renal enzymes, gamma-glutamyl transpeptidase, N-acetyl-beta-glucosaminidase, and alkaline phosphatase. Most of the rats did not demonstrate any significant change in urinary levels of beta-galactosidase. There was a highly significant positive correlation between urinary oxalate and N-acetyl-beta-glucosaminidase.
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PMID:Urinary enzymes and calcium oxalate urolithiasis. 257 Jan 67

Sodium vanadate, an agent known to have multiple cellular actions, was studied for its effects on aspects of bone formation in cultures of 21-day-old fetal rat calvariae. Vanadate (0.1-10 microM) stimulated the incorporation of [3H] thymidine into acid-insoluble residues (DNA); the effect appeared after 3 h and was sustained for 96 h. Vanadate increased the bone DNA content and mitotic index. Treatment with vanadate at 10 microM for 24 h or at 0.3-1 microM for 96 h increased the incorporation of [3H]proline into collagenase-digestible protein (CDP), but the effect was not specific for collagen; vanadate also increased the labeling of noncollagen protein (NCP). Vanadate increased the incorporation of [3H]proline into type I collagen without affecting other collagen types. Vanadate (100 microM) caused a marked and irreversible inhibitory effect on the labeling of DNA, CDP, and NCP. Treatment with vanadate at multiple doses for 3-96 h did not stimulate alkaline phosphatase activity, but this enzyme was inhibited in bones exposed to 1 mM vanadate for 24 h or 10 microM vanadate for 96 h. The stimulatory effect on DNA labeling was primarily observed in the periosteum, while that on CDP labeling was seen only in the periosteum-free bone. These studies indicate that sodium vanadate stimulates bone DNA, collagen, and NCP syntheses in vitro, although high doses of vanadate have an irreversible inhibitory effect.
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PMID:Effect of sodium vanadate on deoxyribonucleic acid and protein syntheses in cultured rat calvariae. 257 50

The present investigation was undertaken to clarify the essential role of zinc on bone protein synthesis in tissue culture. Calvariae were removed from 3-week-old male rats and cultured for periods up to 72 hr in Dulbecco's Modified Eagle Medium (high glucose, 4500 mg/dl) supplemented with antibiotics and bovine serum albumin. The calvariae were incubated for 24 hr at 37 degrees in 5% CO2/95% air in medium containing 10(-6)-10(-3) M dipicolinate, a chelator of zinc, and then the bones were transferred into medium containing either 10(-4) M zinc sulfate or vehicle without dipicolinate. Zinc content in bone tissues was decreased when the culture was treated with 10(-4) and 10(-3) M dipicolinate for 24 hr. When calvariae treated with 10(-4) M dipicolinate for 24 hr were further cultured in medium without dipicolinate for 24 and 48 hr, bone alkaline phosphatase activity was decreased by about 40% (P less than 0.01) of untreated bone enzyme activity. The decreased alkaline phosphatase activity was increased markedly by the presence of 10(-4) M zinc (about 2.5-fold of control value). This effect of zinc was blocked completely by the presence of 10(-7) M cycloheximide, but 10(-8) M actinomycin D caused only a partial inhibition. When calvariae treated with 10(-4) M dipicolinate were pulsed with [3H]proline, the incorporation of [3H]proline into the acid-insoluble residues of bone tissue was decreased by about 40% (P less than 0.01) of the value obtained from calvariae not treated with dipicolinate. The presence of 10(-4) M zinc caused an increase of about 2-fold in [3H]proline incorporation. Bone DNA content was not altered significantly by treatment with 10(-4) dipicolinate or 10(-4) M zinc. These results clearly indicate that endogenous zinc induces the stimulation of protein synthesis at the translational process in bone cells. The present study further supports the view that zinc plays an essential role for protein synthesis in bone cells.
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PMID:Effect of dipicolinate, a chelator of zinc, on bone protein synthesis in tissue culture. The essential role of zinc. 260 49


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