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)

To examine the contribution of exogenous calcium and oxalate in magnesium deficiency, intestinal absorption of both calcium and oxalate was studied by preparing brush border membrane vesicles (BBMV). Purity of the BBMV was ascertained biochemically by enrichment of the marker enzyme alkaline phosphatase by 14-fold with a concomitant 90 per cent decrease in the basolateral marker enzyme Na+/K(+)-ATPase in the purified membrane preparation as compared to the respective homogenate in both the groups. Uptake studies were carried out by a rapid filtration technique. The kinetics were studied by measuring the rate of influx as a function of concentration (0.1-1.0 mM). BBMV from both the groups showed a linear positive relationship between the uptake rate and the concentration for both calcium and oxalate, thereby demonstrating that calcium and oxalate are transported through intestinal microvillus membrane by a simple passive diffusion process. However, the rate of uptake of calcium and oxalate was significantly higher in the magnesium-deficient group as compared to the pair-fed control group, as shown by the increase in the slope line for both calcium and oxalate (for calcium, control = 3.88, deficient = 5.86; for oxalate, control = 4.41, deficient = 7.20). Analysis of the lipid composition of the BBM revealed a significant decrease in the cholesterol content (P < 0.01) with a concomitant increase in the triglycerides (P < 0.01) and total fatty acid content (P < 0.001) in the magnesium-deficient group. Thus the results indicate that, although the mechanism of translocation of calcium and oxalate in the intestine is similar in the two groups, magnesium deficiency leads to hyperabsorption of both the ligands through alterations in the lipid composition of the membrane, thereby increasing the risk of stone formation.
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PMID:Intestinal absorption of calcium and oxalate in magnesium-deficient rats. 839 6

To evaluate the role of parathyroids in calculus disease, the parathyroid hormone levels were determined in 22 control subjects and 42 stone (14 with bladder stone and 28 with kidney stone) patients. Serum calcium, inorganic phosphate, alkaline phosphatase and parathyroid hormone and urinary excretion of calcium and inorganic phosphate were determined. It was found that normocalcemic and normocalciuric stone patients had slightly higher levels of parathyroid hormone (irrespective of the site of the stone) and the difference was not statistically significant as compared with control subjects although some of the patients with calculus disease were hyperparathyroid. Serum alkaline phosphatase was increased while there was an increase in urinary calcium excretion in kidney stone patients and oxalate in all patients as compared with control subjects. The increase in inorganic phosphate was, however, not different from the control subjects. The subclinical hyperparathyroidism and stone formation in these patients are not correlated.
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PMID:Parathyroid hormone in urinary stone patients. 851 Jun 69

Gossypol was administered in Goya olive oil to low protein-fed (LP, protein-malnourished) and normal protein-fed (NP, control) adult male albino Wistar rats for 4 and 8 weeks at 20 mg/kg body weight/rat/day. At the end of the experiment, the rats were killed and blood was drawn from the rats by cardiac puncture and subjected to hematological and biochemical analyses. The data obtained were analyzed by two-way analysis of variance (ANOVA). The interaction of the treatments produced significant effects on serum levels of sodium, potassium, cholesterol, triglyceride, urea, glutamate oxalate transaminase, glutamate pyruvate transaminase, amylase and blood platelet count (P < 0.001), and uric acid (P < 0.01). Significant effects were produced on serum phosphate, albumin and blood reticulocyte count (P < 0.05) but not on packed cell volume, red blood cell count, white blood cell (WBC) count and WBC differential counts, hemoglobin concentration, creatinine, creatinine phosphokinase and alkaline phosphatase (P < 0.05). The administration of gossypol reduced the level of transaminases, cholesterol and uric acid in LP and NP rats, increased the levels of triglycerides, amylase, platelet and reticulocyte count in LP rats but decreased them in NP rats. The implications of the findings are discussed.
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PMID:The blood constituents of gossypol-treated, protein-malnourished Wistar rats. 860 84

Investigations were undertaken to study the role of lupeol, a pentacyclic triterpene from Crataeva nurvala stem bark, in calcium oxalate experimental rat urolithiasis. A 2% solution of ammonium oxalate was administered by gastric intubation for inducing hyperoxaluric condition in adult male rats of Wistar strain. The duration of treatment was for 15 days. This resulted in increased urinary excretion of oxalate associated with reduction in citrate and glycosaminoglycans. The urinary marker enzymes which indicate renal tissue damage namely--lactate dehydrogenase, inorganic pyrophosphatase, alkaline phosphatase, gamma glutamyl transferase, beta-glucuronidase and N-acetyl beta-D glucosaminidase were found to be elevated. Lupeol administration (25 mg/kg body weight/day) reduced significantly the renal excretion of oxalate. It also reduced the extent of renal tubular damage as evidenced from the decreased levels of the above enzymes in urine. Such a reduction is likely to be beneficial in minimizing the deposition of stone-forming constituents in the kidney which provides antilithic effect.
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PMID:Effect of lupeol, a pentacyclic triterpene, on urinary enzymes in hyperoxaluric rats. 871 54

Levamisole inhibits alkaline phosphatase (ALP) activity in kidney brush border membranes and increases phosphate excretion in vivo in dogs and rats. I-p-Bromotetramisole (I-BR) is a more potent analog of levamisole in regard to inhibition of ALP activity in vitro, but had no effect on phosphate transport by in vitro proximal tubules of the rabbit. Since its effect on phosphate excretion in vivo has not been studied, the present study tested the effects of infusion of I-BR on phosphate excretion in Sprague-Dawley rats. Fractional excretion of phosphate (FEPi) was measured in thyroparathyroidectomized Sprague-Dawley rats before and during a systemic infusion at 0.8 ml/min of 10 mM I-p-Bromotetramisole oxalate (I-BR, n = 6), or the inactive isomer d-p-Bromotetramisole oxalate (d-BR, n = 5). The FEPi increased significantly from 4.7% +/- 0.9% to 13.4% +/- 3.1% in response to I-BR whereas there were no changes in FEPi with inactive d-BR. In conclusion, systemic infusion of I-p-Bromotetramisole increases FEPi in Sprague-Dawley rats.
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PMID:Effect of bromotetramisole on renal phosphate excretion. 893 64

The Wilson disease adenosinetriphosphatase (ATPase; ATP7B) is believed to bind copper as Cu(I). We provide evidence to suggest that the ATPase actually transports Cu as Cu(II). When the copper is presented to rat liver microsomes as Cu(I), virtually all uptake is ATP independent. If the copper is presented as copper oxalate [Cu(II)], total uptake is reduced to approximately 10% of Cu(I) levels, but ATP-dependent uptake rises, both as a proportion of total uptake and in absolute terms. The reducing agent vitamin C and the Cu(I) chelator bathocuproine both override the effect of oxalate. The data indicate that there are two transporters in the microsomes, an ATP-independent Cu(I) transporter and an ATP-dependent Cu(II) pump. The activity of the Cu(I) transporter correlates most strongly with alkaline phosphatase, suggesting that it is derived from plasma membrane contamination. Cu(II) ATP-dependent transport correlates only with beta-1, 4-galactosyltransferase, which indicates that it is located in the Golgi apparatus.
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PMID:ATP-dependent copper transporter, in the Golgi apparatus of rat hepatocytes, transports Cu(II) not Cu(I). 894 86

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation.
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PMID:Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture. 901 81

The in vivo effect of cyclosporin A (CsA) on renal calcium oxalate (CaOx) crystal retention in experimental hyperoxaluric rats was investigated. Further, the effect of pretreatment of vitamin E on the above conditions was also studied. Male Wistar rats were divided into two major groups each containing 40 rats. One of the groups was pretreated with vitamin E. Both major groups were then subgrouped into four groups: group 1 received the vehicle (olive oil); group 2 received CsA in olive oil (50 mg/kg); group 3 received 3% ammonium oxalate (AmOx), and group 4 received CsA + AmOx. Nephrotoxicity was assessed by the activities of urinary marker enzymes and also by histopathology. Urinary oxalate excretion as well as the activities of lactate dehydrogenase, gamma-glutamyltranspeptidase, alkaline phosphatase and inorganic pyrophosphatase enzymes were elevated either in CsA-alone or AmOx-alone treated groups. On combined administration of both CsA and AmOx, further elevations of these enzymes were observed. Urinary excretion of oxalate concentration positively correlated with urinary excretion of these enzymes. Deposition of CaOx crystals was seen only in the kidneys of rats that received combined treatment. On pretreatment with vitamin E the observed increased urinary activities of the enzymes and oxalate, histopathological changes and the deposition of CaOx crystals by administration of CsA in hyperoxaluria were prevented suggesting that vitamin E could be supplemented to prevent CsA-induced membrane damage.
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PMID:Vitamin E pretreatment prevents cyclosporin A-induced crystal deposition in hyperoxaluric rats. 903 Dec 74

Nephrocalcin (NC), an acidic glycoprotein with molecular weight 14,000, is present in urine and prevents kidney stone formation. Histoimmunochemical staining shows that NC is localized in the proximal tubles in kidneys. Isolated NC from mammalian urine, revealed at least 4 isoforms of NC (we call these isoforms NC-A, NC-B, NC-C, and NC-D in the order of elution) during DEAE cellulose column chromatography with a linear gradient of NaCl elution step. Non-stone forming people excrete more NC-A and NC-B isoforms in urine; however, more NC-C and NC-D isoforms were found in stone formers' urine. When the organic matrix was extracted from surgically removed calcium oxalate kidney stones, we found greater quantities of NC-C and NC-D isoforms than those of NC-A and NC-B isoforms. Amino acid compositions and carbohydrate contents of these 4 isoforms were similar with the exception of the gamma-carboxyglutamic acid (GLA) residues. Only the NC-A and NC-B isoforms contained residues of GLA. There were more phosphate residues present in NC-C and NC-D than in NC-A and NC-B. Upon removal of phosphate residues by alkaline phosphatase, NC-C eluted at the same salt concentrations as NC-A eluted. This indicates that the backbone protein could be similar, but the NC-C isoform is modified by excess phosphate residues. Surface tension measurements using a Lauda film balance indicated that NC-A and -B were strongly amphiphilic while NC-C and -D were less amphiphilic. NC-A has an elongated shape, and occupies a smaller area per molecule; whereas NC-C is a bulky molecule. Using NC-A as a model of a "good" inhibitor and NC-C as a model of a "poor" inhibitor, both bound with 4 atoms of Ca2+ per molecule as investigated by equilibrium dialysis method, 31P-NMR, and electron spin resonance spectrometry. Isoforms A and B changed their conformation upon Ca2+ binding, but C and D did not change their conformation. All these observations suggest that isoforms A and B are strong inhibitors of calcium oxalate monohydrate (COM) crystal growth and aggregation. However, isoforms C and D act as promotors for COM crystal growth-kidney stone formation. Measuring the amount of NC in urine from renal cell carcinoma patients and from NC isolated from a supernatant of a primary renal cell carcinoma cells demonstrated the amount of NC increased with disease progression.
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PMID:Properties and function of nephrocalcin: mechanism of kidney stone inhibition or promotion. 909 76

The role of lipid peroxidation (LPO) in renal tubular damage mediated calcium oxalate retention was investigated in a rat model. Hyperoxaluria, without deposition of oxalate in kidney, was induced by administration of ethylene glycol (EG), a precursor of oxalate. Oxidative stress condition was produced by administration of buthionine sulfoximine (BSO), an inhibitor of glutathione biosynthesis. BSO-treated rats showed a significant (p < 0.001) increase in LPO over EG-treated rats and it was almost doubled in BSO + EG treated rats. LPO was accompanied by significant urinary excretion of renal damage marker enzymes such as gamma-glutamyl transpeptidase (gamma-GT), alkaline phosphatase (ALP) and cathepsin D, mucoproteins, and glycosaminoglycans (GAGs) in the BSO and BSO + EG groups but not in the EG group. Urinary excretion of gamma-GT (r = +0.90) (p < 0.001) and deposition of oxalate (r = +0.78) (p < 0.001) in kidney positively correlated with LPO. These results suggest that LPO initiates renal damage, thereby leading to calcium oxalate retention and stone formation.
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PMID:Renal injury mediated calcium oxalate nephrolithiasis: role of lipid peroxidation. 915 57


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