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)

Most of the alkaline phosphatase activity in the mouse uterus during early pregnancy was found to be membrane-bound and was associated with particulate material when homogenates were centrifuged at 105 000 g. The activity of the enzyme increased in both the particulate and cytosol fractions of uterine homogenates during early pregnancy to reach maximum values on day 7 of pregnancy. Studies of the enzyme in its membrane-bound and cytosolic forms before and after solubilization with Triton X-100, and n-butanol failed to detect any evidence that the membrane microenvironment or membrane are deeply buried within the membranes of uterine cells. Thus, the properties of the enzyme in response to amino acids, inhibitors, and Mg2+ and Zn2+, and changes in pH, substrate concentration and temperature were essentially unaltered when the phosphatase was present in a membrane-bound or cytosolic form, or when fractions were treated with Triton X-100 and n-butanol. Solubilized preparations of the enzyme from particulate and cytosol fractions of uterine homogenates displayed zones of activity with similar anodal migration rates during electrophoresis on cellulose acetate membranes suggesting that the cytosolic activity may arise from particulate material during homogenization of the tissue. Several amino acids stimulated the activity of the phosphatase while cysteine, histidine, homoarginine, Na2HPO4 and 4-(p-aminophenylazo)phenylarsonic acid were inhibitory. In addition, Km values for the enzyme from all uterine fractions hydrolysing p-nitrophenyl phosphate were temperature-dependent.
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PMID:Behaviour and properties of membrane-bound mouse uterine alkaline phosphatase during early pregnancy. 721 59

Acetazolamide, furosemide, ethacrynic acid and chlorothiazide, diuretics of considerable structural diversity, inhibit alkaline phosphatase. The inhibition is reversible and the mechanism is of the mixed type, having both competitive and non-competitive characteristics. Ki is calculated to be 8.4, 7.0, 2.8 and 0.1 mmol/l for acetazolamide, furosemide, ethacrynic acid and chlorothiazide, respectively. Chlorothiazide is a much more potent inhibitor of alkaline phosphatase than the other three diuretics. The combination of ethacrynic acid and cysteine, itself an alkaline phosphatase inhibitor, is less inhibitory than ethacrynic acid alone. Rat and human kidney alkaline phosphatase are equally sensitive to chlorothiazide, ethacrynic acid and furosemide.
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PMID:Inhibition of alkaline phosphatase by several diuretics. 735 51

The activity of alkaline phosphatase (AAP) in papillary capillaries of normal and psoriatic skin was characterized by enzyme inhibition studies. Quantitatively, there were pronounced differences between normal and psoriatic skin, i.e., increase of AAP, as determined by a grading system, and assimilation of the strength of AAP in venous and arterial side of the capillary loop in psoriasis. Qualitatively, the inhibition studies with different actin inhibitors revealed no difference between AAP in normal and psoriatic skin or between initial, fully developed and healed psoriatic lesions as well as noninvolved skin of psoriatics. Thus, the physiologic AAP seems to be stimulated in psoriasis. Generally, AAP of dermal capillaries is highly sensitive to cysteine inhibition.
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PMID:Characterization of activity of alkaline phosphatase (AAP) in capillary endothelium of normal and psoriatic skin. 740 28

A histochemical investigation has been made to localize and characterize various lipid, protein, carbohydrate and enzyme constituents present within the different cell types of the epidermis of Anabas testudineus. The polygonal cells contain glycogen, the amount of which gradually increases as the cells move towards the surface until they reach the most superficial layer where the amount of glycogen slightly decreases indicating the metabolically active state of these cells. The basal cells, which frequently undergo cell proliferation, contain no glycogen. The polygonal cells give strong reactions for SDH, alkaline phosphatase, cholesterol esters and nonsulphated acid mucopolysaccharides, moderate reactions for acidic lipids, phospholipids and free cholesterol and weak reactions for neutral mucopolysaccharides, protein bound NH2 groups, mucoprotein, tyrosine, tryptophan and cysteine bound sulphydryl groups. These cells in the outermost layer give stronger reactions for acidic lipids, phospholipids and cholesterol esters and weaker reactions for SDH and alkaline phosphatase activities. The above findings reveal that the polygonal cells remain metabolically active throughout the epidermis. The mucous cells are numerous and secrete mixture of neutral mucopolysaccharides, sulphated acid mucopolysaccharides and nonsulphated acid mucopolysaccharides. The contents of the sacciform granulated cels are mainly proteins. A thick coat of slime over the body surface containing mucopolysaccharides, lipids and proteins is important in keeping the skin moist and may facilitate the survival of the fish while it is on land. The melanophores in the epidermis may playing important role in preventing the colinization by parasites, fungi and bacteria over the body surface, act as macrophages.
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PMID:A histochemical study of the epidermis of the climbing perch, Anabas testudineus (Anabantidae, Pisces). 742 82

We studied two monoclonal antibodies (MAbs 9-11 and 41-1) which are specific for dominant and conserved epitopes located on HIV-1 transmembrane Gp41. These MAbs recognize both Gp41 and a synthetic HIV-1 envelope peptide (39GC) which is a fragment of Gp41. The interactions between MAbs 9-11 and 41-1 and 39GC either coupled to a sensor chip or to alkaline phosphatase were investigated using BIAcore technology. The association and dissociation rate constants as well as the affinity constants were determined. BIAcore technology allows real-time determination of the interaction between two molecules without the need for any labeling, neither isotopic nor enzymatic. The peptide 39GC was immobilized by coupling to dextran on the BIAcore biosensor through a disulfide bond with a cysteine residue added to the N-terminus of the synthetic peptide. The two native cysteine residues located in the loop of Gp41 were protected by ethylcarbamoyl residues (CONHC2H5); this chemical modification prevented the formation of the S-S bridge and in particular the internal loop. We specifically studied the interaction between the MAbs and either the protected peptide or the peptide whose cysteine residues had been deprotected in situ by alkaline treatment. The results showed that MAb 41-1 recognized 39GC either protected (Ka = 7.6 x 10(6) M-1) or unprotected (Ka = 1.48 x 10(8) M-1), whereas MAb 9-11 recognized only the unprotected form (Ka = 2.18 x 10(8) M-1). Our results suggest that the epitope MAb 9-11 is directed against a part of the peptide sequence which includes the two native cysteines. The difference in affinity observed for MAb 41-1 between the protected and the unprotected forms of 39GC was found to be due to a lower rate of dissociation for unprotected 39GC; these results illustrate the importance of peptide conformation on antibody recognition and might be explained by a conformational change due to reconstitution of the internal loop following deprotection of the thiol groups. MAbs 9-11 and 41-1 also recognized 39GC conjugated to alkaline phosphatase and deprotected. We observed a difference between the rate constants for MAb 41-1 binding to free peptide and its binding to the peptide-enzyme conjugate which might be due to changes in peptide flexibility. In contrast, the rate constants of MAb 9-11 were the same in both experiments, suggesting that the rigidity of the internal loop prevents changes in 9-11 epitope conformation.
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PMID:Effect of HIV-1 peptide presentation on the affinity constants of two monoclonal antibodies determined by BIAcore technology. 751 68

Male Swiss OF1 mice were administered orally with a single dose (200 mg/kg) of 1,1-dichloroethylene (DCE). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 50% of the proximal tubules at 8 h following DCE administration. Pretreatment with the anionic transport inhibitor probenecid by i.p., (0.75 mmol/kg, 30 min prior to and 10 min and 5 h following DCE administration) and with the gamma-glutamyltranspeptidase (GGT) inactivator acivicin by gavage and i.p. (50 mg/kg, 1 h and 30 min prior to DCE administration) failed to prevent DCE-induced renal toxicity. Pretreatment with the beta-lyase inactivator amino-oxyacetic acid (AOAA) by gavage (100 mg/kg, 30 min prior to and 10 min and 5 h following DCE administration), and with the renal cysteine conjugate S-oxidase inhibitor methimazole by i.p. (40 mg/kg, 30 min prior to DCE administration) reduced the number of damaged tubules by approximately 50 and 60%, respectively in mice treated with DCE. The results suggest that the DCE undergoes biotransformation by NADPH-cytochrome P450 to several reactive species which conjugate with glutathione (GSH). After arriving in the kidneys, the resulting conjugates reach the renal cells by a mechanism which depends on neither GGT, nor on an anionic transport system which is sensitive to probenecid. Once in the cells, the presumed GSH conjugates and/or their derivatives undergo secondary modification by beta-lyase and cysteine conjugate S-oxidase to reactive metabolite(s).
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PMID:Nephrotoxicity mechanism of 1,1-dichloroethylene in mice. 761 82

Cisplatin, a nephrotoxic chemotherapeutic agent, was injected into Sprague Dawley rats, alone or together with cysteine, vitamin E and clonidine. The effects on erythrocyte fragility, serum composition, and kidney and liver enzymes were studied. Cisplatin was administered as two i.p. injections (6 mg/kg body weight) at an interval of 120 hours. The animals were sacrificed 24 hours after the second injection. Erythrocytes were prepared from blood collection with anticoagulant. Serum was prepared from clotted blood, collected without anticoagulant. Kidneys and liver were removed and homogenized, and a supernatant prepared by high speed centrifugation. In cisplatin-treated rats, the serum activities of aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase and alkaline phosphatase were significantly decreased, whereas the activities of isocitric dehydrogenase and glutathione reductase were increased. Also, concentrations of blood urea nitrogen, creatinine, total lipids and magnesium increased while albumin and glucose decreased. Mean osmotic fragility of erythrocytes from cisplatin-treated rats was decreased, while the haematocrit was increased. In the liver, the only change seen was an increased activity of isocitric dehydrogenase. Much greater changes were found in the kidneys, with increased activity of glucose-6-phosphate dehydrogenase and decreased activities of aspartate and alanine aminotransferases, alkaline phosphatase, malic dehydrogenase, sorbitol dehydrogenase and gamma-glutamyltransferase, as well as a decreased phosphorylation to oxidation ratio in the mitochondria, indicating reduced adenosine triphosphate production. Administration of cysteine and vitamin E together with cisplatin partially reversed the uraemia and many of the biochemical changes induced by cisplatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum, liver and kidneys of cisplatin-treated rats; effects of antioxidants. 788 81

Leukemia inhibitory factor (LIF) is a pleiotropic cytokine with both anabolic and catabolic effects on bone tissue. To investigate the effect of LIF on bone formation in the absence of a resorption cycle, we used fetal rat calvaria cell cultures and quantified bone nodule production, which provides a colony assay to analyze the effects of factors on osteoprogenitor differentiation and bone formation. In these cultures, dexamethasone (Dex) stimulates bone nodule formation. In dose-response experiments, LIF inhibited bone nodule formation by cells cultured with (+Dex; ID50 = 250 U/ml) or without (-Dex; ID50 = 30 U/ml) 10(-8) M Dex. Residual nodules were small and poorly mineralized. Continuous exposure to LIF (500 U/ml) up to day 25 did not affect either the growth rate or saturation density of the cultures, but decreased alkaline phosphatase activity and bone nodule production, with greater inhibition in -Dex cultures. Exposure to LIF (500 U/ml) for 3 days early during nodule formation (about day 10) reduced bone nodule numbers to the same extent as continuous treatment in -Dex cultures and significantly, but less markedly, in +Dex cultures; earlier and later pulses had no effect. Northern blot analysis of expression of messenger RNAs of bone related proteins in cultures pulsed (-Dex) at various stages of development showed marked inhibition of alkaline phosphatase, bone sialoprotein, and osteocalcin; slight inhibition of type I collagen; early stimulation of osteopontin; and no effect on Secreted Protein, Acidic and Rich in Cysteine/osteonectin. These results suggest that LIF is an inhibitor of bone nodule formation in these cultures, acting at a stage when late osteoprogenitors and/or early osteoblasts are present, and that Dex may modulate the effects of LIF by shifting effective doses to higher concentrations.
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PMID:Leukemia inhibitory factor inhibits osteogenic differentiation in rat calvaria cell cultures. 789 51

Male Swiss OF1 mice were injected subcutaneously with 20 mg/kg of cis-platinum (II) diamine dichloride (cis-platin). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 10, 20, 40 and 50% of the proximal tubules after 7, 24, 48 and 72 h, respectively. Pretreatment with the glutathione synthesis inhibitor, buthionine sulfoximine (BSO), (i.p. 3 mmol/kg) potentiated the tubule damage of cis-platin. In contrast, pretreatment with organic anion transport inhibitor probenecid (i.p. 3 x 0.75 mmol/kg) reduced the number of damaged tubules by approximately 80% at 72 h after cis-platin injection. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator acivicin (AT-125, 50 mg/kg p.o., plus 50 mg/kg i.p.) failed to prevent cis-platin induced renal toxicity. Pretreatment with the beta-lyase inactivator aminooxyacetic acid (AOAA, 2 x 100 mg/kg p.o.) and with the renal cysteine conjugate S-oxidase inhibitor methimazole (40 mg/kg i.p.) reduced the number of damaged tubules by approximately 40% and 75%, respectively in mice treated with cis-platin. The results suggest that the platinum-sulfhydryl group complexes formed are taken up by the kidney cells through an organic anion transport mechanism which is probenecid-sensitive. In the cells these complexes are stable for several hours, depending on the intracellular glutathione (GSH) level, and gradually undergo transformation to reactive metabolite(s) by renal intracellular beta-lyase and S-oxidase.
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PMID:Nephrotoxicity mechanism of cis-platinum (II) diamine dichloride in mice. 790 24

Activity hydrolyzing both N omega-phosphoarginine and glucose-6-phosphate was detected in rat renal microsome but not in hepatic microsome. Renal microsome was solubilized with 1% n-octyl-beta-D-thioglucoside and purified with DEAE-Sepharose column chromatography. Fractions hydrolyzing both N omega-phosphoarginine or glucose-6-phosphate were subjected to 7.5%-polyacrylamide gel electrophoresis in the presence of 0.1% sodium dodecyl sulfate. Phosphatase activity in the gels was detected by a lead nitrate stain using N omega-phosphoarginine or glucose-6-phosphate as substrates. Both substrates produced a stain in the region of the gel corresponding to a protein with a mass of 150 kDa. Extracts of slices from this region of the gel also hydrolyzed phosphocreatine, inorganic pyrophosphate, and O-phosphotyrosine. Moreover, the phosphatase had its optimal pH in the alkaline range and was inhibited completely by 20 microM sodium vanadate, 1 mM cysteine, and 1 mM tetramisole. All these properties indicate that the microsomal phosphoamidase (EC 3.9.1.1) of rat kidney was identical with alkaline phosphatase (EC 3.1.3.1).
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PMID:N omega-phosphoarginine phosphatase from rat renal microsome was alkaline phosphatase. 803 Nov 15


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