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)

We measured the excretion rates of six urinary enzymes that either originate from the proximal renal tubule, like alanine aminopeptidase (EC 3.4.11.2), alkaline phosphatase (EC 3.1.3.1), gamma-glutamyltransferase (EC 2.3.2.2), and N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30), or that are typical low-molecular-mass proteins, like lysozyme (EC 3.2.1.17) and pancreatic ribonuclease (EC 3.1.27.5). These rates were compared with those of total protein and albumin in urine of 36 insulin-dependent diabetic men and 30 healthy men. Seventeen of the diabetics had "clinical proteinuria," defined as excretion of more than 7.5 g of protein per mole of urinary creatinine (group B). Group A comprised the 19 diabetics without proteinuria. Except for gamma-glutamyltransferase, the excretions of enzymes and proteins were significantly higher in diabetics than in controls and were greater in group B than in group A. N-Acetyl-beta-D-glucosaminidase was the analyte most often increased in group A (89%), followed by albumin and alkaline phosphatase (each 32%). All patients in group B showed increased excretion of N-acetyl-beta-D-glucosaminidase. We conclude from the comparative data that this enzyme may be useful as an early predictor of diabetic nephropathy.
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PMID:Urinary enzymes and low-molecular-mass proteins as indicators of diabetic nephropathy. 289 6

Two days after cisplatin was injected into rats, urinary N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyltranspeptidase (gamma-GTP) activities increased. The urinary excretion of NAG continued to rise until 4 days after the injection of cisplatin, the last day examined. However, the increase in urinary gamma-GTP excretion which lasted for 2 days returned to its control level 4 days after cisplatin injection. The alkaline phosphatase activity in urine was unaffected by cisplatin injections. The antioxidant N-N'-diphenyl-p-phenylenediamine attenuated these increases in enzyme activities caused by cisplatin. The results of this study suggest that monitoring the change in urinary activities of some enzymes is the method of choice for detecting cisplatin nephrotoxicity and that the increase may involve the generation of free radicals by cisplatin.
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PMID:Effect of N-N'-diphenyl-p-phenylenediamine pretreatment on urinary enzyme excretion in cisplatin nephrotoxicity in rats. 289 7

As a first step in studies on the molecular mechanism(s) underlying gentamicin toxicity, the effect of treating rats with this aminoglycoside antibiotic (100 mg/kg once or twice daily for 3 days) on the analytical subfractionation of the kidney cortex has been examined. DNA was used as a marker for the nuclei, cytochrome oxidase for mitochondria, acid phosphatase for lysosomes, catalase for peroxisomes (with reservations; see the companion paper), NADPH-cytochrome c reductase for the endoplasmic reticulum, p-nitrophenyl-alpha-mannosidase (at pH 5.5) for the Golgi apparatus, AMPase for the plasma membrane in general and alkaline phosphatase for the brush border, and lactate dehydrogenase for the cytosol. In addition, the presumptive lysosomal hydrolases N-acetyl-beta-D-glucosaminidase, p-nitrophenyl-alpha-mannosidase (at pH 4.5), cathepsin D, and DNase II were monitored. Electron microscopy was also performed on the subfractions obtained. The only significant biochemical changes brought about by gentamicin treatment were that N-acetyl-beta-D-glucosaminidase demonstrated both a greater total activity and a larger enrichment in the 104,000gav pellet, while p-nitrophenyl-alpha-mannosidase at pH 4.5 demonstrated the same total activity and a greater enrichment in the 104,000gav pellet. Since myeloid bodies were shown by electron microscopy to sediment primarily with the 500gav and 10,000gav pellets, the biochemical changes seen cannot be associated with these morphological structures. These findings suggest that selective changes in a certain subpopulation(s) of lysosomes or in certain lysosomal enzymes may be involved in the early stages of gentamicin toxicity. On the other hand, no lysosomal membrane damage was observed here, since both the latency of acid phosphatase and the recovery of this activity in the soluble cytosol were unchanged. The present investigation may also have relevance for the dosage and duration of gentamicin treatment chosen in clinical situations.
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PMID:Biochemical effects of gentamicin on rat kidney cortex. II. Analytical subfractionation after short-term, high-dose treatment. 303 Aug

The nephrotoxicity of three different dose levels of propyleneimine (10, 20 and 30 microliter/kg body wt) administered intraperitoneally to rats was studied and 20 microliters/kg body weight was found to be the most appropriate sublethal dose. Injection of propyleneimine (10 microliters/kg body wt) produced a small rise in N-acetyl-beta-D-glucosaminidase (NAG) activity, minor histological damage but no change in urine volume. Six rats were injected with 20 microliters/kg body weight, and urine was collected over the following 16 days. An immediate increase in urine volume, osmolality together with a concomitant decrease in specific gravity, was accompanied by a small increase in creatinine excretion and a more marked increase in the sodium and potassium content of urine after the administration of the nephrotoxin. NAG activity increased immediately and peaked on day 3, the activity remained elevated until day 12 when it fell to near normal levels. The activity of both beta-D-galactosidase and beta-D-glucosidase increased 9 days after administration of the nephrotoxin. In contrast, no consistent change was found in the excretion of the brush border marker enzymes, leucine aminopeptidase (LAP), alanine aminopeptidase (AAP) or alkaline phosphatase (ALP). Proteinuria increased sharply the day after injection and remained abnormal. Increased urinary albumin excretion and the predominance of low molecular weight proteins was demonstrated by sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. Evidence is presented that propyleneimine exerts its early toxic effect on the renal papilla.
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PMID:Renal toxicity of propyleneimine: assessment by non-invasive techniques in the rat. 309 1

In order to establish sensitive methods of detecting minor renal damage, changes of enzymes, tubular cell counts, and creatinine in the urine were investigated in rats that had been given nephrotoxic chemicals. Daily administration of mercuric chloride (HgCl2) dose-dependently increased urinary excretions of lactate dehydrogenase (LDH), aspartate aminotransferase (GOT), alkaline phosphatase (ALP), leucine aminopeptidase (LAP), lysozyme (LZM), N-acetyl-beta-D-glucosaminidase (NAG), and acid protease together with increased counts of tubular cells in the urine. The increase in tubular cell counts and the change in urinary LDH isoenzyme profile preceded the changes in the other enzymes. Daily administration of gentamicin (GM) increased urinary excretions of LDH, GOT, LZM, NAG, acid protease and tubular cell counts in a dose-dependent manner, but did not increase gamma-glutamyl transpeptidase (gamma-GTP) and ALP excretions. The urinary isoenzyme profiles of LDH in rats treated with GM were different from those with HgCl2. The increase in acid protease excretion outlasted those in LDH and GOT in the high dose group. It was concluded that the severity of renal damage can be readily detected by periodic determinations of the following urinary parameters: tubular cell counts, LDH isoenzyme, acid protease, LZM and NAG, in addition to either LDH or GOT and one of the enzymes ALP, LAP or gamma-GTP. Furthermore, the site of renal damage can be presumed from these results.
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PMID:Urinalysis for detection of chemically induced renal damage (1)--Changes in urinary excretions of enzymes and various components caused by mercuric chloride and gentamicin. 344 39

In order to establish sensitive methods of detecting minor renal damage, changes of enzymes, protein, tubular cell counts, and creatinine in the urine were investigated in rats to which nephrotoxic chemicals had been administered. Daily administration of p-aminophenol (PAP) dose-dependently increased urinary excretions of lactate dehydrogenase (LDH) and its isoenzymes (LDH5 = LDH4 greater than LDH3 greater than LDH2 = LDH1), aspartate aminotransferase (GOT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), leucine aminopeptidase (LAP), lysozyme (LZM), N-acetyl-beta-D-glucosaminidase (NAG) and acid protease together with increased counts of tubular cells in the urine. Tubular cell counts, LDH and GOT were more sensitive indicators in the PAP tubulonephritis. Single i.v. injection of puromycin aminonucleoside (PM) dose-dependently increased urinary excretions of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 = LDH4 greater than LDH3), GOT, NAG, acid protease and protein but degree of the increases in these enzymes was lower than those in the rats treated with PAP. PM increased excretions of high molecular weight proteins but did not increase ALP, gamma-GTP, LAP, LZM and tubular cells excretions. Single i.v. injection of hexadimethrine increased urinary excretion of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 greater than LDH3 = LDH4), GOT, LZM, NAG and acid protease together with increased counts of tubular cells in the urine but did not increase ALP, gamma-GTP and LAP excretions. It is concluded that tubular cell counts, LDH isoenzymes and battery of these enzymes in urine are useful markers for detecting the severity and the site of renal damage in addition that urinary protein is a useful marker for detecting glomerular damage.
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PMID:Urinalysis for detection of chemically induced renal damage (2)--Changes in urinary excretions of enzymes and various components caused by p-aminophenol, puromycin aminonucleoside and hexadimethrine. 344 40

The catalytic activities of alkaline phosphatase and N-acetyl-beta-D-glucosaminidase, constituents of luminal brush-border membranes and lysosomes of kidney tubular cells, were measured in human kidney allografts in the maintenance and recovery phases of acute renal failure and in acute rejection crisis. The enzyme activities were fluorometrically determined in single microdissected cortical nephron segments of biopsies from 4 kidney allografts taken intraoperatively and postoperatively at different periods, which exhibited either good function or dysfunction. For comparison, the unaffected part of a human kidney nephrectomized due to hypernephroma as well as a biopsy of a morphologically normal human kidney were examined. Both enzymes displayed highest activities in the proximal part of the human nephron. In some intraoperative and postoperative biopsies with acute renal failure, alkaline phosphatase activity was reduced in proximal tubules, predominantly in the straight portion. This reduction could not be correlated with function. In acute rejection, very low alkaline phosphatase activities were uniformly found in proximal convoluted and straight tubules. Furthermore, intraoperative biopsies and biopsies of the functioning allograft have only approximately 50% of normal N-acetyl-beta-D-glucosaminidase activity in proximal convoluted tubules, but generally normal values in the straight portion. However, in acute renal failure, this enzyme activity was several-fold enhanced along the whole nephron, when compared with intraoperative values. In acute rejection, N-acetyl-beta-D-glucosaminidase activity was slightly reduced in proximal convoluted tubules, when compared with biopsies showing good function. It is suggested that the decrease of proximal tubular enzyme activities is the consequence of increased enzymuria and inadequate enzyme regeneration. On the other hand, the overshoot of N-acetyl-beta-D-glucosaminidase activity in the maintenance phase of acute renal failure appears to indicate increased degradative capacity, associated with cellular regeneration along the whole nephron.
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PMID:Catalytic activities of alkaline phosphatase and N-acetyl-beta-D-glucosaminidase in human cortical nephron segments: heterogeneous changes in acute renal failure and acute rejection following kidney allotransplantation. 354 86

Biopsy specimens from 29 adenomas, 17 adenocarcinomas, and 6 synchronous adenomas in cancer patients and from uninvolved mucosa of all main segments of the large bowel were examined histologically and assayed for a series of organelle marker enzymes. Six enzymes--lactase, sucrase, alkaline phosphatase, 5'-nucleotidase, acid phosphatase, and N-acetyl-beta-D-glucosaminidase--showed less activity in adenomas than in adjacent uninvolved mucosa and in specimens from controls. Cancer tissue had higher gamma-glutamyltransferase and lower lactase, alkaline and acid phosphatases, and N-acetyl-beta-D-glucosaminidase activities than specimens from uninvolved mucosa in cancer patients and control patients. Enhanced alkaline phosphatase and N-acetyl-beta-D-glucosaminidase activities were seen in uninvolved mucosa of cancer patients as compared with those of adenoma and control patients. Evidence has been found for multienzyme analysis to identify adenomas with signs of malignant transformation and carcinomas with poor prognosis.
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PMID:Enzyme activities in biopsy specimens from large-bowel mucosa in colorectal adenomas and carcinomas. 362 77

To evaluate a critical concentration concept of cadmium (Cd) toxicity on the kidney, relationships of renal Cd level with urinary excretion of various substances--i.e., metallothionein, alkaline phosphatase, lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase, total protein, Cd, copper, and zinc--were studied in Cd-injected rats. At the renal Cd concentration of 100-200 micrograms/g tissue, a dramatic increase of all these substances in urine was observed, supporting the idea of the critical concentration proposed by Friberg and co-workers (1974). The significance of increase of urinary metallothionein below this level is also discussed.
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PMID:Critical concentration of cadmium for renal toxicity in rats. 368 16

In rabbits inflammation of the cornea was induced by intrastromal injection of horse serum. Between 2 and 4 weeks after injection, infiltration of the cornea with leukocytes and neovascularization could be observed. During this period, the rabbits were killed and their corneas analyzed for protein, alkaline phosphatase, acid phosphatase, N-acetyl-beta-D-glucosaminidase, and lactate dehydrogenase. The enzyme activities in the inflamed corneal stroma reflect the high lysosomal activity, which probably originates from the leukocytes. The enzyme activities in the epithelium indicate that the tissue is abnormal and undergoing repair processes.
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PMID:Enzyme activities in the rabbit cornea during immunogenic keratitis. 371 Jan 83


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