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)

The human nephrotic syndrome (NS) is accompanied by important alterations of mineral and bone metabolism. The purpose of the present study was to examine bone metabolism in rats with experimental NS and normal creatinine clearance, and to evaluate the reversibility of this alteration. NS was induced by three injections of puromycin aminonucleoside (PAN) on days 0, 21, and 35 (10, 5, and 5 mg/100 g body weight, respectively). The biochemical markers of bone formation (osteocalcin and alkaline phosphatase) and bone resorption (hydroxyproline and pyridinoline), bone mineral content (BMC), and bone mineral density (BMD), determined by dual-energy x-ray absorptiometry (DEXA), were studied on days 0, 7, 14, 28, 42, 56, 84, and 112. Proteinuria was present throughout the study. Hypoproteinemia was seen on days 7, 28, 42, and 56, returning to control values on days 84 and 112. In serum, osteocalcin (OC) concentration increased (p < 0.001), and alkaline phosphatase (ALP) decreased (p = 0.002). In urine, hydroxyproline increased (p < 0.001), but urinary pyridinoline was not different from the control group throughout the study. Increased serum parathyroid hormone concentration and decreased levels of 25-hydroxy and 1,25-dihydroxyvitamin D were found from day 7. During the intense proteinuria, bone resorption predominates and decreased BMC and BMD ensues in PAN-nephrotic rats. PAN-nephrotic rats showed low BMC and BMD compared to control group (p < 0.001). At the end of the study, when proteinuria persisted but total serum protein returned to control values, the biochemical bone markers, BMC, and BMD returned to normal. In conclusion, PAN-nephrotic rats had reversible bone alterations that were related to the magnitude of proteinuria and the concentration of total serum protein.
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PMID:Biochemical bone markers, bone mineral content, and bone mineral density in rats with experimental nephrotic syndrome. 915 58

Clinical, haematological and pathological studies were undertaken in Jordan in a stud of 103 racing horses clinically suffering from babesiosis and apparently healthy animals. Out of 47 horses which participated in strenuous exercise, three mares showed sudden onset of immobility and reluctance to move and two mares died. Clinical examination revealed that these five horses (group 1) had fever, anorexia, weakness and severe icterus and, in two mares, haemoglobinuria. Haematological examination revealed that all five horses were heavily parasitized with Babesia equi. This was also found in four horses (group 2) with no evidence of clinical babesiosis. In group 3 (94 horses), neither clinical signs nor B. equi were observed in the blood. The horses in group 1 and 2 recovered after treatment with imidocarb. When the mean values of white blood cell count, red blood cell count, haemoglobin and packed cell volume in group 1 were compared with those for groups 2 and 3, a significant difference was found (P < 0.05). A significant difference was also found when the mean values were compared before and after treatment. Examination of serum total protein, bilirubin and serum enzymes revealed a significant decrease in the mean value of total serum protein (P < 0.05), and a significant increase in the mean values of bilirubin (P < 0.05) in group 1 compared to groups 2 and 3. A significant elevation in the mean value of aspartate aminotransaminase, gamma-glutamyltransferase and creatine phosphokinase and a substantial elevation in the mean value of alkaline phosphatase was also observed in group 1 compared to groups 2 and 3. Postmortem examination of the dead horses showed that the animals had icterus, hepatomegaly and full urinary bladder with deep-red urine. Histopathological examination of the liver showed massive centrilobular degeneration and necrosis. The bile canaliculi and bile ducts were prominent and plugged with dark-brown to canary-coloured bile pigments. The lungs had congestion, oedema, and thrombosis of pulmonary veins. Our results suggest that the horses suffered from B. equal with clinical manifestation following exercise. The clinical, haematological and pathological findings indicate that the animals suffered from haemolytic anaemia which responded to imidocarb therapy.
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PMID:Equine babesiosis associated with strenuous exercise: clinical and pathological studies in Jordan. 918 24

We describe the effects on cell function of treating porous bioactive glass (BG) such that its surface is a composite of carbonated hydroxyapatite and serum protein. The effects on bone cell function of porous hydroxyapatite (HA) ceramic and porous glass treated to become amorphous calcium phosphate only also were studied subsequent to their having adsorbed a serum protein layer. Substrates treated for different durations were seeded with MC3T3-E1 cells and cultured for 3-17 days. Whereas cells seeded on any substrates, BG and HA produced collagen types I and III, bone sialoprotein, and osteopontin, there were significant differences between HA and BG, and among the various surface conditions created on BG. Covering the glass surface with hydroxyapatite and serum protein enhanced expression of high alkaline phosphatase activity, high rates of cell proliferation, and production of mineralized extracellular matrix. The enhancement may be due to the adsorption of a high quantity of fibronectin from the serum onto the reacted bioactive glass surface.
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PMID:Porous bioactive glass and hydroxyapatite ceramic affect bone cell function in vitro along different time lines. 926 78

Swiss albino rats were treated in groups with CCl4, and flyash to induce cellular toxicity in the lungs and trachea. Animal groups received treatment of Koflet (K) with CCl4 (7 days) and with flyash (30 days); their general health and biochemical parameters were studied and used as an indication of cellular injuries. A significant loss was observed in body weight and food consumption in animals given only CCl4 or flyash, while simultaneous treatment with K resulted in a non significant alteration from normal control groups. Enzyme (alkaline phosphatase, Ca2+ -Mg2+ -ATPase, glutamic-oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT)) activities were estimated in tissue homogenate preparation of lung, trachea and serum, which showed no significant change except for GPT activity as compared to control animals which received CCl4 or flyash with K. Similarly lung, trachea and serum contents of carbohydrate, protein, sialic acid, serum protein, serum cholesterol were estimated and it was found that alteration caused by CCl4, or flyash becomes almost non-significant compared to that of the control after the treatment of K, except for carbohydrate and serum cholesterol values. The animal group which was only treated with K did not show any significant alteration in their biochemical markers or injuries, except for cholesterol.
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PMID:In vivo protective role of Koflet (an ayurvedic preparation) against cellular toxicity caused by CCl4 and flyash. 940 99

The kinetic method revealed that by the rate of adsorption on apatite, serum alkaline phosphatase (AlP) is homologous and salivary AlP consists of two fractions: "slow" with the constant of adsorption rate approximating that of serum AlP and "fast" with 5-6 times greater constant. A mechanism of phosphatase immobilization on apatite by two-stage sequential reaction is proposed. The constants of rates of both stages for the serum phosphatase and fast salivary fraction are determined. Difference of the products of both stages by the Michaelis constant (KM) is demonstrated for the fast fraction. The KM of the second-stage immobilization product is close to that of AlP immobilized on dental enamel, which confirms the hypothesis about their identity. In contrast to AlP, both serum and salivary alpha-amylase react with apatite at the same rate and, probably, by the same mechanism as the bulk of salivary and serum protein.
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PMID:[The possible mechanisms of alkaline phosphatase and alpha-amylase immobilization in dental enamel]. 947 22

Case records of 27 dogs with medically managed congenital portosystemic shunts were reviewed. Fourteen were followed up by telephone questionnaires to the owners. Age, breed, sex, clinical signs and blood results were similar to previous studies. Weight and quality of life were stable or improved on treatment in all cases. Total serum protein concentration and alanine aminotransferase and alkaline phosphatase activities fell significantly during treatment. Fourteen dogs were euthanased, four were lost to follow-up and nine remained alive. Mean survival time for the dogs euthanased was 9.9 months. Mean follow-up period for the dogs still alive was 56.9 months and all had survived more than 36 months from diagnosis. Surviving dogs with intrahepatic shunts had a significantly shorter follow-up period than dogs with extrahepatic shunts. Two prognostic indicators were identified, age at initial signs and blood urea concentration on presentation, both correlating with survival time. It was demonstrated that a significant proportion of dogs with portosystemic shunts managed medically have a good prognosis.
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PMID:Medical management of congenital portosystemic shunts in 27 dogs--a retrospective study. 951 85

Preliminary short-term toxicity studies of sucrose acetate isobutyrate (SAIB) in the dog demonstrated that addition of this additive to the diet was associated with an increase in liver size and elevated serum alkaline phosphatase activity with no evidence of pathological change by light microscopy. To determine the basis for these changes, a 12-week oral toxicity study of SAIB was conducted in the dog and a similar study was performed in the rat. SAIB was fed in the diet to groups of six beagle dogs of each sex at 0, 0.5, 1.0, 2.0 and 4.0%. SAIB was also fed to groups of 40 Sprague-Dawley rats of each sex at levels of 0, 2.5, 5.0 and 10.0%. In the rat study, in addition to routine toxicology parameters, hepatic microsomal enzyme induction was determined using a zoxazolamine hypnotic test, urinary ascorbic acid excretion and determination of hepatic carboxylesterase activity. Sodium phenobarbital was fed to groups of 20 rats of each sex at a dose of 100 mg/kg body weight/day by gavage as a positive control for hepatic microsomal enzyme induction. In the dog study, routine toxicological tests were supplemented by tests for bromsulfophthalein (BSP) retention, histochemical staining of liver sections for glycogen, phosphorylase, succinate dehydrogenase, and acid and alkaline phosphatases. Levels of liver lipid, protein, glycogen and carboxylesterase activity were also determined. Electron microscopic examinations were made on liver sections from the dog study at the end of the 12-week SAIB feeding period and after a 2-week withdrawal period. Administration of SAIB to rats did not reveal evidence of any effect on hepatobiliary function, and there was no indication of microsomal enzyme induction. Body weight gain of male rats fed SAIB was decreased, probably as the result of decreased palatability of the diet; SAIB did not affect body weight gain in females. The changes observed in the dogs fed SAIB included increased serum alkaline phosphatase activity with no change in serum alanine aminotransferase, aspartate aminotransferase or lactic dehydrogenase activity and no change in serum electrolyte, serum protein, glucose or bilirubin levels. No haematological changes were observed. BSP retention was observed at all SAIB dose levels. There were no SAIB-related pathological changes in any organ when examined by light microscopy. Examination by electron microscope revealed dilatation of bile canaliculi and an increase in smooth endoplasmic reticulum compared with controls. Histochemical studies also indicated increased enzyme activity of the bile canaliculi. The electron-microscope-revealed changes were completely reversed during a 2-week treatment withdrawal period. The dog study did not establish a no-effect level for changes in hepatobiliary function induced by feeding SAIB.
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PMID:Subchronic toxicity studies of sucrose acetate isobutyrate (SAIB) in the rat and dog. 951 48

The effect of two new chelating agents-Tiron (4,5-dihydroxy-1,3-benzene disulphonic acid disodium salt) and succinic acid--on the mobilization of beryllium was studied. Animals were exposed to beryllium nitrate (1 mg kg(-1) i.p.) daily for 21 days. Administration of beryllium nitrate showed a marked decrease in haemoglobin percentage, blood sugar, serum alkaline phosphatase and serum protein and a significant increase in the activity of transaminases. Tissue protein and glycogen contents and the activity of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase showed significantly decreased values, but beryllium nitrate provoked a considerable increase in the activity of acid phosphatase and glucose-6-phosphatase in the vital and reproductive organs. Significant improvement in the haematological and biochemical parameters was observed with Tiron but no therapeutic effect was seen with succinic acid. Atomic absorption spectrophotometry (AAS) also showed a decreased level of beryllium concentration in the liver and kidney after Tiron therapy.
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PMID:Influence of chelating agents on the toxicity and distribution of beryllium in rats. 980 33

A probable outbreak of oak (Quercus calliprinos) toxicosis in a herd of beef cattle--heifers and first-calving cows--grazing in the Judean foothills of Israel is described. Toxicosis probably occurred because of the consumption of oak leaves and buds during a period of pasture scarcity without any feed supplementation. A progressive syndrome of wasting, dullness, anorexia, polyuria, nephrosis, constipation and recumbency, culminating in death, was seen. A high mortality rate of 83% (38/46 animals) was noted. The clinical-pathological findings revealed increases in blood urea, creatinine, aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), creatine kinase (CK), lactate dehydrogenase (LDH) and inorganic phosphorus. Decreases were found in alkaline phosphatase (ALP), total serum protein, albumin (ALB), triglyceride (TG), calcium (Ca), magnesium (Mg), sodium (Na) and chloride (CI). The main pathological findings were severe nephrosis, chronic interstitial nephritis, and occasional intestinal ulceration. On the basis of epidemiology, clinical signs, clinical-pathological and pathological findings and renal histology, a tentative diagnosis of oak toxicosis was made.
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PMID:Probable toxicosis in cattle in Israel caused by the oak Quercus calliprinos. 983 Jun 93

Osteoporosis is a common problem of aging and results from a failure of homeostatic mechanisms to regulate osteogenesis and mineralization. Bovine and human forms of fetuin glycoprotein bind to the transforming growth factor (TGF)-beta/BMP (bone morphogenic protein) cytokines and block their osteogenic activity in cell culture assays (Demetriou, M., Binkert, C., Sukhu, B., Tenenbaum, H. C., and Dennis, J. W. (1996) J. Biol. Chem. 271, 12755-12761). Fetuin is a prominent serum glycoprotein and a major noncollagenous component of mineralized bone in mammals. In this study, we show that recombinant fetuin and native serum protein have similar potency as inhibitors of osteogenesis in dexamethasone-treated rat bone marrow cell cultures (dex-RBMC). Recombinant bovine fetuin also bound to TGF-beta1 and BMP-2 in vitro with kinetics similar to native fetuin. Although TGF-beta1 is required for osteogenesis in dex-RBMC, the cytokine also inhibited osteogenesis at concentrations >/=10 pM. Titration of fetuin or anti-TGF-beta1 antibodies into the bone marrow cultures in the presence of 10 pM TGF-beta1 restored osteogenesis, whereas titrations of the same reagents into cultures with 0.3 pM added TGF-beta1 were inhibitory, confirming the biphasic nature of the TGF-beta1 response. Suppression of osteogenesis by both TGF-beta1 and the antagonist proteins required their presence within the first 6 days of culture, well before mineralization at 10-12 days. Northern analysis showed that both fetuin and high dose TGF-beta1 suppressed expression of the bone-associated transcripts alkaline phosphatase, osteopontin, collagen type I, and bone sialoprotein. The suppression of osteogenesis by fetuin and by high dose TGF-beta1 was accompanied by the differentiation of an alternate cell lineage with adipocyte characteristics. In summary, the biphasic osteogenic response to TGF-beta1 suggests that overlapping gradients of TGF-beta/BMP cytokines and fetuin regulate osteogenesis in remodeling bone.
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PMID:Regulation of osteogenesis by fetuin. 1049 15


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