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)

A kinetic study of the inhibition of several alkaline phosphatase (AP isoenzyme activities by phenobarbital was carried out using p-nitrophenylphosphate (10 mM) as a substrate at pH 9.8 in a 300-mM Hepes buffer. AP from bovine kidney, calf intestine, bovine liver, and rat bone was used. Over a phenobarbital concentration range of 20-400 mM, all these isoenzymes were inhibited in an uncompetitive manner with a Ki of 200 mM for intestinal AP, and in a linear mixed-type manner for all the other isoenzymes tested. The Ki values were 10, 40 and 55 mM for kidney, bone and liver AP, respectively. The use of 15 mM carbonate-bicarbonate or 400 mM diethanolamine buffer did not modify the degree of inhibition of intestinal AP activity. Dixon plots of the reciprocal of reaction velocity versus inhibitor concentration either at different substrate concentration or at different DEA concentration indicate uncompetitive inhibition for the intestinal enzyme. This in vitro inhibitory effect of phenobarbital is in contrast to its in vivo stimulating action on AP. However, in the whole animal, the effects of phenobarbital administration probably represent the sum of multiple effects.
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PMID:In vitro inhibition of alkaline phosphatase activities from intestine, bone, liver, and kidney by phenobarbital. 130 51

A major goal of the combined effort of basic scientists and plastic and reconstructive surgeons is the development of novel bone substitutes based on osteogenic growth and differentiation factors with optimal delivery systems for skeletal repair. Osteogenin is a protein initiator of bone differentiation. The present study examined the osteogenic potential of osteogenin in combination with porous hydroxyapatite replicas obtained after hydrothermal conversion of calcium carbonate exoskeletons of corals. Bovine osteogenin, with an apparent molecular weight of 28 to 42 kDa, purified by hydroxyapatite-Ultrogel adsorption chromatography, heparin-Sepharose affinity chromatography, and HR Sephacryl S-200 molecular sieve chromatography, was delivered into rods of nonresorbable and resorbable hydroxyapatite replicas with an average porosity of 600 microns. A total of 48 rods were bioassayed for osteogenic activity by intramuscular implantation into eight adult baboons (Papio ursinus) as a prerequisite for clinical trials in humans. Bovine osteogenin fractions reconstituted with baboon insoluble collagenous bone matrix were implanted in an additional four adult baboons. Specimens were harvested at 30 and 90 days after implantation and subjected to histomorphometry and alkaline phosphatase activity determination. Differentiation of bone occurred in nonresorbable hydroxyapatite rods, both osteogenin-treated and controls. However, no bone formation was observed in resorbable rods, even in the presence of osteogenin. These results demonstrate that the surface and chemical characteristics of the substratum, independent of the osteogenic stimulus, have a profound influence on the morphogenesis of bone. The demonstration of bone induction in nonhuman primates with porous nonresorbable hydroxyapatite replicas and baboon insoluble collagenous bone matrix reconstituted with bovine osteogenin establishes the therapeutic potential of the principle of bone induction in craniofacial, periodontal, and orthopedic reconstructive surgery.
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PMID:Induction of bone in composites of osteogenin and porous hydroxyapatite in baboons. 131 41

The use of oral calcium carbonate as a phosphate binder is often complicated by hypercalcaemia, particularly with concomitant use of vitamin D analogues. We previously found that stepwise reduction of dialysate calcium effectively countered this complication in haemodialysis patients, and have now assessed the strategy in CAPD patients. Seventeen patients underwent conversion from aluminium hydroxide to calcium carbonate and were followed for 5 months, with subsequent addition of alfacalcidol for a further 5 months. Standard CAPD dialysate (1.75 mM calcium) was used, reducing to 1.45 mM and, if necessary, to 1.00 mM in patients who became hypercalcaemic. While receiving calcium carbonate alone, 12 of the 17 patients became hypercalcaemic, this responding in four to dialysate calcium reduction to 1.45 mM. In the remaining eight patients, further reduction to 1.00 mM was required and in two patients even this failed to control hypercalcaemia adequately, necessitating reversion to aluminium hydroxide. Phosphate control remained unchanged, as did calcium x phosphorus product. There were transient increases of blood ionised calcium, and decreases of parathyroid hormone, with progressive reduction of serum aluminium and alkaline phosphatase. The addition of alfacalcidol (0.25 microgram/day) led to hypercalcaemia in six subjects, successfully countered by dialysate calcium reduction in four. The results show that standard CAPD dialysate calcium at 1.75 mM is too high for the majority of calcium carbonate treated patients and that substantial reductions of the dialysate calcium concentration are required if calcium carbonate is to be used effectively.
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PMID:Dialysate calcium reduction in CAPD patients treated with calcium carbonate and alfacalcidol. 131 83

Due to toxic side effects of aluminum-containing agents for treatment of uremic hypophosphatemia, much interest has been focused upon aluminum-free phosphate binder alternatives. From results of experimental studies with calcium acetate, this salt has been suggested as a possible effective and safe phosphate binder. In the present study, calcium acetate was used during a mean of 11 months for serum phosphate control in 30 uremic patients previously treated with aluminum and/or calcium carbonate. Satisfactory control of serum phosphate was achieved during the study (mean phosphate concentration +/- SE: 2.15 +/- 0.12 mmol/l compared to prestudy 2.23 +/- 0.19 mmol/l). Mean serum concentrations of calcium, alkaline phosphatase and parathyroid hormone did not change significantly during the study. Serum aluminum decreased significantly (p less than 0.01). Moderate hypercalcemia was observed in 6 patients. Calcium acetate treatment was withdrawn in 2 patients due to gastrointestinal discomfort. It is concluded that calcium acetate seems to be an effective phosphate binder alternative with relatively few side effects.
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PMID:Calcium acetate used as phosphate binding treatment in uremic hyperphosphatemia. 168 Apr 30

The calcium balance of 12 presumed healthy human young adult subjects was assessed. Subjects consumed a constant laboratory-controlled diet supplemented with one of four calcium-fortified food products: orange juice (OJ), milk (M), experimental pasteurized processed cheese (T), soda (S), or a calcium carbonate plus vitamin D tablet (CC). Study length was 6 weeks with seven-day experimental periods (2-days allowed for adjustment with 5-days combined for purposes of analysis). All urine and fecal samples were collected by the subjects for the duration of the study. Blood samples were drawn at the end of each experimental period. Urine and fecal calcium contents were determined. Blood samples were analyzed for alkaline phosphatase. Results of this study indicate a higher fecal calcium content (mg/day) when subjects consumed CC and T, and when subjects consumed self-selected diets, than when given S, M, or OJ. Urinary calcium excretion was significantly lower when subjects consumed OJ than when they consumed M, T, or their self-selected diets. A significantly larger positive calcium balance was demonstrated when subjects consumed OJ as compared to T. Fecal transmit time did not vary significantly. Serum alkaline phosphatase was significantly lower when subjects consumed T than when they consumed self-selected diets.
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PMID:Calcium bioavailability from calcium fortified food products. 176 36

The present review summarizes the characteristics of renal bone disease in pediatric patients treated with maintenance peritoneal dialysis. Fifty-eight patients underwent iliac crest bone biopsy after double tetracycline labeling, measurements of aluminum in bone and various serum biochemical determinations including serum PTH, alkaline phosphatase, calcium, phosphorus and aluminum. Evidence of osteitis fibrosa was present in 45% of patients and mild lesions of secondary hyperparathyroidism were found in an additional 25%. Thus, secondary hyperparathyroidism remains the predominant bone lesion despite the use of oral calcitriol. Evidence of aluminum accumulation was substantially less prevalent, findings not surprising due to the widespread use of calcium carbonate as the main phosphate binder agent. However, aplastic bone lesion without aluminum staining was present in the majority of patients with low-turnover lesions of the bone without osteomalacic findings. The long-term evolution of such lesions remains to be evaluated. The potential value of alternative modes of calcitriol administration for the control of secondary hyperparathyroidism is discussed as well as the differences in the bioavailability of sterol according to the different routes for calcitriol administration.
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PMID:Renal bone disease in pediatric patients receiving treatment with maintenance peritoneal dialysis. 177 95

Development of the mineralization process in the course of atherogenesis was studied using the cholesterol-fed rabbit model. The aorta samples were investigated by means of proton and electron microprobes, infrared spectroscopy and X-ray diffraction as well as selected histochemical staining. Blood serum was analysed every 2 weeks to determine the content of cholesterol, triglycerides, inorganic phosphorus, ionized calcium, elemental composition as well as activity of alkaline phosphatase. It was found that the administered diet did not disturb the calcium and phosphorus homeostasis. Histochemical findings confirmed the formation of lipid-rich lesions blocking the lumen of the vessel. The dystrophic calcification was observed only in the atheroma, while in the tunica media a slight mineralization similar to that found in controls was observed after 210 days of the diet. In the atheroma the only phase detected was a defective hydroxyapatite. The perfection of the crystals, as well as the diameter of the deposits, increased during the course of the diet reaching about 2 microns after 210 days. The crystals were not contaminated with carbonate groups regardless of the duration of the diet.
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PMID:Calcification of aortic wall in cholesterol-fed rabbits. 185 64

Bone mineral content, estimated by single-photon absorptiometry of the forearm, serum values of intact parathyroid hormone (PTH(1-84], osteocalcin, alkaline phosphatase, 1,25-dihydroxycholecalciferol (1,25(OH)2D3), and aluminium were determined during treatment with calcium carbonate (CaCO3) or aluminium hydroxide (Al(OH)3) in 11 dialysis patients participating in a randomised cross-over study. Each treatment period lasted 6 months. Serum phosphorus was maintained in the range 1.5-2.0 mmol/l. During Al(OH)3 treatment bone mineral content (BMC) decreased by 11% per half-year (mean), but only by 3% per half-year during CaCO3 treatment (P less than 0.05). Comparing the CaCO3 and Al(OH)3 periods the following differences were found: serum calcium increased during CaCO3 treatment, PTH(1-84) decreased (79% of initial values during CaCO3 versus 196% during Al(OH)3, mean area under curve, P less than 0.05), osteocalcin decreased (89% versus 117%, P less than 0.01), alkaline phosphatase decreased (92% versus 116%, P less than 0.05), and aluminium decreased (56% versus 189%, P less than 0.05). 1,25(OH)2D3 remained unchanged in both periods. No increase in soft-tissue calcification was demonstrated on X-ray of the shoulders in any of the periods. Thus, CaCO3 treatment seems to slow down loss of bone mineral content, and using CaCO3 as phosphate binder may have a more beneficial effect on the progression of uraemic bone disease than Al(OH)3 due to the reduction of hyperparathyroidism and bone turnover.
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PMID:Comparison of calcium carbonate and aluminium hydroxide as phosphate binders on biochemical bone markers, PTH(1-84), and bone mineral content in dialysis patients. 185 34

The investigation was carried out on 12 cows and their calves. At the time of 3 months before parturition and 7 days after parturition metabolic alkalosis one provoked with the high protein feed. The laboratory investigations dependent of determinations on the rumen content the pH, NH3, volatile fatty, acids, the protozoa, bacteria, total gas CO2 and CH4. On the arterial and venous blood on determination the pH, BE, sO2, pO2, HCO3 and coefficient of consumption of the oxygen, and on the venous blood the levels of Na, K, Mg, Ca, P, total proteins, albumins and globulins, cholesterol, glucose, bilirubin, alkaline phosphatase and urea. In the colostrum and in milk one determined the pH, potential acidosis--degree SH, proper weight, proteins, dried mas of milk, time of coagulation in the presence of rennin, Na, K, Ca, Cl, total fats and their composition with different fatty acids. No existed truly changes of clinical signs, only feces was sickly. The metabolic alkalosis of cows decreased the consumption of oxygen across the tissue, deficient of the energy, disorders of water-electrolyte and acid-base balances. The calves form cows with metabolic alkalosis delivered also with metabolic alkalosis, with the symptoms of achondroplasia and degeneration of the liver and other organs. Metabolic alkalosis of cows influenced on the quality of colostrum and milk. The colostrum gained from cows with alkalosis caused of disturbance of gastrointestinal tract and diarrhea presence.
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PMID:[The effect of metabolic alkalosis on colostrum and milk quality of cows and on the health status of their newborns]. 188 61

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
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PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37


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