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)

Excretion patterns of kidney related urinary proteins such as lysosomal beta-N-acetylglucosaminidase (beta NAG), brush-border Ala-(Leu-Gly)-aminopeptidase (AAP), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (AP) as well as of IgG, albumin, and alpha-1-microglobulin, were assessed in patients with chronic glomerulonephritis (n = 53), pyelonephritis (n = 27), systemic lupus erythematodes (n = 5), and patients with essential arterial hypertension (n = 18). Excretion of tubular marker enzymes and serumproteins (related to urine creatinine concentration = protein creatinine index) in spontaneously voided second morning urine was significantly higher as compared to the controls (n = 2). Alpha-1-microglobulin was markedly elevated in both pyelonephritis and glomerulonephritis indicating disturbance in tubulointerstitial handling of microglobulins also in cases with primary glomerulopathy. Rise of albumin, IgG, and alpha-1-microglobulin as well as of tubular kidney markers AAP, AP, GGT, and beta NAG in cases with arterial hypertension without preexisting nephropathy support the hypothesis of a defect in charge and size permselectivity in these patients which is probably due to an increase in glomerular capillary perfusion pressure and hyperfiltration.
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PMID:Kidney- and serum derived proteins in urine of patients suffering from renal diseases or arterial hypertension. 247 9

Renal toxicity is the major side effect of cis-dichlorodiammine platinum (CDDP) and it develops renal tubular damage. In the present study, the acute changes of urinary beta-glucuronidase (beta-GL) and alkaline phosphatase (ALP) activities following CDDP administration as indicators of its toxicity were studied in 5 patients with urological malignant tumors. The activities were measured for 11 days continuously from the day before CDDP administration. In all cases, both urinary enzyme activities increased with CDDP administration. Increase patterns of urinary beta-GL activities were similar to those of urinary NAG, but remarkably-high values of beta-GL activities were found in cases of urothelial tumors probably because urinary beta-GL derives from the kidney (lysosomes of tubular cells) and from the epithelial cells of urinary tract. Urinary ALP activities changed corresponding well with urinary gamma-glutamyl transpeptidase (gamma-GTP). This study shows that the determination of urinary beta-GL is not a significant marker of CDDP renal toxicity, especially in cases with urological malignancies, in contrast to results for urinary brush border enzyme activities such as ALP or gamma-GTP.
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PMID:[Study on urinary beta-glucuronidase and alkaline phosphatase activities as indicators of CDDP renal toxicity]. 272 12

Excretion of urinary lactate dehydrogenase (LDH, EC 1.1.1.27), gamma-glutamyltransferase (gamma-GT, EC 2.3.2.2), alkaline phosphatase (ALP, EC 3.1.3.1), alanine aminopeptidase (AAP, EC 3.4.11.-), alanine aminotransferase (GPT, EC 2.6.1.2) and N-acetyl-beta-D-glucosaminidase (NAG, EC 3.2.1.30) was studied following a single i.v. application of 1 mg mercuric chloride/kg body weight or a radio contrast medium (SH H 340 AB) at a dose of 7.5 g iodine/kg body weight in rats. Measurements of urinary enzymes and serum urea nitrogen and creatinine were carried out on the second, third, fourth and ninth days after treatment. Histological examinations of kidneys were performed on day 9. A drastic increase in urinary LDH and moderate increase in gamma-GT, ALP and AAP and a very slight increase in GPT was observed in the first 18-h urine samples after mercuric chloride. This increase in enzymuria was associated with a drastic increase in serum urea nitrogen and creatinine, with a maximum on day 4. The radio contrast medium-treated animals showed a similar but less pronounced pattern of urinary enzymes excretion and only a slight increase of serum urea nitrogen on day 2. A good correlation was found between histological findings and enzymuria as well as serum urea nitrogen and creatinine. Thus, determination of only some urinary enzymes (LDH and gamma-GT) is valuable in predicting early nephrotoxicity and sufficient for the diagnosis of proximal tubule damage in rats.
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PMID:Value of enzyme determinations in urine for the diagnosis of nephrotoxicity in rats. 287 61

We have studied in rats the influence of renal ischemia on urinary excretion of three brush border membrane enzymes (gamma glutamyl transferase, alkaline phosphatase and leucine aminopeptidase) and of a lysosomal one (N-acetyl-B-D-glucosaminidase). Urines were collected over 24 hours periods during three days before and after a 45 minutes renal artery clamping. Urinary GGT, PAL and LAP excretion were significantly increased on the first day after renal ischemia, but returns to normal values on the second day. Urinary NAG activity increases on the first day, but contrary to the latter enzymes, reached to normal values only on the third day. Enzymuria seems to be a useful marker of tubular injury occurring after a temporary renal ischemia in the rat.
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PMID:[Importance of urinary enzymes as a marker of post-ischemic proximal tubular involvement in rat]. 288 19

beta-D-Glucuronidase (EC 3.2.1.31) was purified to homogeneity from human spleen, and enzyme fractions from CM-Sephadex were examined for uptake by fibroblasts and retention by a column of immobilized phosphomannosyl receptor. Uptake and binding were enhanced by treatment of the enzyme with alpha-N-acetylglucosaminyl phosphodiesterase, greatly reduced by prior treatment with alkaline phosphatase, and restored by subsequent treatment with alpha-N-acetylglucosaminyl phosphodiesterase. Immobilized phosphomannosyl receptor was used to separate high and low uptake enzyme forms. About 25% of the total beta-glucuronidase was retained by the receptor column and eluted with mannose 6-phosphate. The rate of uptake of retained enzyme was 2.5-3.0-fold greater than that of the enzyme applied to the receptor column. The fraction retained by the column was reduced to 5-10% by prior treatment of the enzyme with alkaline phosphatase. This phosphatase-resistant, receptor-retained fraction was taken up at only 24% the rate of non-phosphatase-treated, receptor-retained enzyme. However, its uptake was increased 7-fold by treatment with alpha-N-acetylglucosaminyl phosphodiesterase. The enhanced rate of pinocytosis conferred by treatment of the enzyme with alpha-N-acetylglucosaminyl phosphodiesterase was destroyed by a subsequent treatment with alkaline phosphatase. These studies demonstrate that although most of the "high uptake" enzyme in beta-glucuronidase from human spleen binds to receptors through phosphomonoesters of mannose, a significant fraction can interact with immobilized phosphomannosyl receptor and be taken up by fibroblasts through interactions involving mannose 6-phosphate in diester linkage with N-acetyl-D-glucosamine.
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PMID:Human beta-glucuronidase pinocytosis and binding to the immobilized phosphomannosyl receptor. Effects of treatment of the enzyme with alpha-N-acetylglucosaminyl phosphodiesterase. 630 37

Ligatin, a receptor that recognizes phosphorylated sugars, was isolated from plasma membranes of mouse macrophages, rat ileum, and rat brain. Several acidic hydrolases including N-acetyl beta-D-glucosaminidase (beta-NAG) were solubilized with this receptor. The solubilized beta-NAG bound to ligatin in vitro as demonstrated by affinity chromatography using the immobilized receptor. beta-N-Acetyl D-glucosaminidase-ligatin complexes were dissociated by low concentrations of mannose 6-phosphate (Man6P) and/or glucose 1-phosphate (Glc 1P). The effectiveness of these two phosphomonosaccharides varied depending on the source of the enzyme: ileal beta-NAG-ligatin complexes showed a four-fold preferential dissociation with Man6P; macrophage complexes showed a 160-fold preferential dissociation with Glc 1P. Brain complexes dissociated with nearly equal preference for Man6P and Glc 1P. Heterologous complexes displayed the specificity characteristic of the source of the enzyme regardless of the source of the ligatin. Treatment of the solubilized hydrolases with endoglucosaminidase H released phosphorous-32 label from these enzymes and prevented binding of beta-NAG to ligatin. However, treatment of the solubilized hydrolases with alkaline phosphatase reduced the binding of beta-NAG to ligatin by no more than 30%. This apparent resistance of beta-NAG to dephosphorylation was consistent with the chromatographic behavior of QAE of 3H-labeled acidic oligosaccharides isolated from the solubilized hydrolases. The oligosaccharides that contain phosphorylated hexose were less acidic than phosphomonoesters and were insensitive to alkaline phosphatase until subjected to acid hydrolysis. These results suggested the presence of a phosphodiester on beta-NAG analogous to the NAC glucosamine 1 P6 mannose present on beta-glucuronidase isolated from mouse lymphoma cells (Tabas I, Kornfield, S: J Biol Chem 255: 6633, 1980).
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PMID:Ligatin binds phosphohexose residues on acidic hydrolases. 729 41

Aminoglycosides, among the most commonly used antibiotics in neonates, have frequently been implicated in nephrotoxic reaction. Studies in adults have indicated that phospholipiduria (PLU) is rapidly increased during aminoglycoside therapy, in relation to the renal phospholipidosis these drugs are known to induce in renal cortex. We studied the effect of amikacin (AK) on PLU in male prematurely-born neonates (gestational age > 34 weeks; postnatal age < or = 2 days) by assessing the urinary excretion of 4 enzymes (N-acetyl-beta-D-glucosaminidase [NAG], alkaline phosphatase, tau-glutamyltransferase and alanine aminopeptidase) and 4 low-molecular-weight proteins (beta-2-microglobulin, clara cell protein, microalbumin and retinol-binding protein) which are currently used to monitor the development and extent of renal tubular damage. Twenty-two patients and 8 healthy (as control) neonates were enrolled in the study. Patients were treated with AK (15 mg/kg per day) given in one (qd, n = 10) or two equal injections (b.i.d., n = 12) for durations of 7-11 days. PLU and proteinuria were determined in 24-h urine sample collections, and enzymes were assessed in spot urine collected at 9 a.m. We found that in neonates, AK causes a significant increase in PLU, and in enzymuria except for NAG in the qd group. Proteinuria showed no significant change due to AK treatment. No significant differences were observed between qd and b.i.d. administrations of AK for all parameters tested. We conclude that PLU could be used in neonates as well as in adults as a non-invasive method to monitor the development of the renal phospholipidosis during aminoglycoside therapy.
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PMID:Urinary phospholipids excretion in neonates treated with amikacin. 767 71

Intestinal-type alkaline phosphatase (IAP) has been localized to the S3 segment of the renal tubule in previous studies, a site believed to be particularly vulnerable to toxic and ischaemic damage. During a 17-month period a pilot study of the value of urinary enzyme measurements (IAP and tissue non-specific alkaline phosphatase--TNAP, using monoclonal antibody-based immunoassays, and N-acetyl-beta-glucosaminidase--NAG, using colorimetric assay) in 50 prospectively followed cases of acute renal failure (ARF) was performed. Urinary enzymes were measured at initial evaluation ('start'), and then each day for 14 days, with the highest enzyme value ('peak') also used for analysis. Patients were divided into prerenal (n = 16), renal (n = 28), postrenal (n = 6) categories according to standard criteria. Of the renal ARF patients 23 of 28 had acute tubular necrosis (ATN), 3 of 28 acute interstitial nephritis (AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50 had a fatal outcome and 1 of 50 was dialysis-dependent at discharge ('poor' prognosis group), while 31 of 50 survived hospital without becoming dialysis-dependent ('good' prognosis group). Median enzyme concentration were increased in 'poor' compared to 'good' prognosis patients: start IAP 3.2 versus 2.2 U/g creat (NS), start NAG 48.6 versus 13.7 (P < 0.01), start TNAP 3.5 versus 0.9 (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary enzymes in acute renal failure. 839 30

The direct effects of cadmium on the functions and metabolism of renal tubular epithelial cells were observed with radio-immune assay, cytochemical and biochemical methods to study further the mechanism of nephrotoxicity of cadmium. Results revealed uptake of alpha-methyl-D-glucoside (alpha-MG) in renal tubular epithelial cells obviously reduced, outflow of potassium ions increased, c-AMP content reduced and activity of Na+-K+-ATPase was inhibited significantly after exposure to cadmium. Electrochemical gradient of tubular cells maintained by Na+-K+-ATPase played an important role in transference of sodium and glucose, and damage in energy resource system within tubular epithelial cells may be one of the pathogenic mechanisms of kidney injury caused by cadmium. In addition, changes in a group of biological markers and functional enzymes (alkaline phosphatase, AKP; gamma-glutamyltransferase, gamma-GT; lactate dehydrogenase, LDH; glucose-6-phosphate dehydrogenase, G-6-PD; N-acetylglucoside, NAG) were determined in the study, and it was found that they all could reflect better the degree of injury in tubular epithelial cells and their metabolic status and could be used in clinical practice.
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PMID:[Toxicity of cadmium and its mechanism on renal tubular epithelial cells in vitro]. 875 54

Wheat germ agglutinin (WGA) precipitates bone type serum alkaline phosphatase (sALP) isoenzyme specifically. The precipitates are composed of the macromolecules of WGA and "bone type sALP" (WGA-ALP complex). In order to use bone type sALP as a marker in polyacrylamide gel electrophoresis (PAGE), a method to separate "bone type sALP" from the "WGA-ALP complex" was established by using N-acetyl-D-glucosamine (GlcNAc)-Sepharose 6E column chromatography. It was concluded that this method is useful for clinical examination in the rat.
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PMID:Identification of rat serum alkaline phosphatase isoenzyme by means of wheat germ agglutinin. 902 78


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