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)

Diversion of portal blood in congenital portosystemic shunts (CPSS) results in liver atrophy and passage of toxins into the systemic circulation causing hepatic encephalopathy. In some dogs, there is indirect evidence for hepatic insufficiency, but histologic findings are equivocal. This study determined whether hepatocyte integrity in PSS is comprised at a subcellular level using analytical subcellular fractionation of liver biopsies. Six dogs with CPSS had hypoproteinemia (6/6), increased serum alkaline phosphatase (6/6) and alanine aminotransferase (4/6) activity, hypocholesterolemia (6/6), and decreased blood urea (2/6). Liver biopsy specimens had increased activities (mU/mg protein) of alkaline phosphatase (17.9 +/- 10.1; controls 5.1 +/- 5.3: P less than 0.01), but not of other plasma membrane enzymes. There were increased activities of endoplasmic reticular (neutral alpha-glucosidase: 1.67 +/- 0.7; controls 0.86 +/- 0.2: P less than 0.01) and lysosomal enzymes (N-acetyl-beta-glucosaminidase: 12.6 +/- 2.3; controls 6.24 +/- 2.7: P less than 0.01; alpha-mannosidase: 0.85 +/- 0.5; controls 0.39 +/- 0.3: P less than 0.05). Subcellular fractionation on reorientating sucrose density gradients showed a high-density peak of alkaline phosphatase suggestive of a specific increase in the biliary canalicular component of enzyme activity. Neutral alpha-glucosidase was shifted to denser fractions, indicative of an increase in the proportion of rough-to-smooth endoplasmic reticulum and consistent with enhanced synthesis of membranous enzymes. There was also evidence for increased fragility of intracellular organelles, particularly lysosomes. In contrast, histology showed either no abnormalities or minor degenerative changes compatible with hepatic underperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic organelle pathology in dogs with congenital portosystemic shunts. 161 98

Enzymes liberated by growing dermatophytes are of pathogenetic importance in tinea. To investigate the influence of nutrients on this enzyme release, Trichophyton rubrum was grown in media containing peptone, keratin and lipids, to which glucose was added in separate assays. The culture supernatants were compared for extracellular enzyme activities by use of the api-zym-test. Our results clearly show that the extracellular enzyme activity is dependent on the nutrients supplied. Seven different enzymes were released when keratin was supplied, as compared to only 5 and 2, respectively, when lipids or peptone were available. Among these enzymes alkaline phosphatase and N-acetyl-beta-glucosaminidase were detected in all cultures lacking glucose. Enzyme release was inhibited completely when glucose was added to the media, except for N-acetyl-beta-glucosaminidase in peptone cultures. This dependency of enzyme release on fungal nutrition can be expected to occur in vivo, too. In addition, it has to be considered for in vitro cultural conditions. Alkaline phosphatase and acetyl-glucosaminidase may be more important in tinea than has been assumed so far.
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PMID:[The enzyme release by Trichophyton rubrum is dependent on nutritional substance supply]. 172 32

Enzymes liberated by growing dermatophytes are of pathogenetic importance in tinea. To investigate the influence of nutrients on this enzyme release, Trichophyton rubrum was grown in media containing peptone, keratin and lipids, to which glucose was added in separate assays. The culture supernatants were compared for extracellular enzyme activities by use of the api-zym test. Our results clearly show that the extracellular enzyme activity is dependent on the nutrients supplied. Seven different enzymes were released when keratin was supplied, as compared with only five and two respectively when lipids or peptone were available. Among these enzymes alkaline phosphatase and N-acetyl-beta-glucosaminidase were detected in all cultures lacking glucose. Enzyme release was inhibited completely when glucose was added to the media, except for N-acetyl-beta-glucosaminidase in peptone cultures. This dependency of enzyme release on fungal nutrition can be expected to occur in vivo too. In addition, it has to be considered for in vitro cultural conditions. Alkaline phosphatase and acetylglucosaminidase may be more important in tinea than has been assumed so far.
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PMID:Enzyme release by Trichophyton rubrum depends on nutritional conditions. 172 75

Single intraperitoneal injections of three, seven, or 10 mg. of sodium oxalate per 100 gm. of rat body weight were administered to male Sprague-Dawley rats. At various times after the injection, urine samples were analyzed for oxalate, and urinary enzymes, alkaline phosphatase, leucine aminopeptidase, gamma-glutamyl transpeptidase, and N-acetyl-beta-glucosaminidase. The kidneys were processed for light microscopy and renal calcium and oxalate determination. Oxalate administration resulted in an increase in urinary oxalate and formation of calcium oxalate crystals in the kidneys. The amount and duration of urinary excretion of excess oxalate and retention of crystals in the kidneys correlated with the dose of sodium oxalate administered. At a low oxalate dose of three mg./100 gm., crystals moved rapidly down the nephron and cleared the kidneys. At higher doses crystals were retained in kidneys and at a dose of 10 mg./100 gm. were still there seven days post-injection. Crystal retention was associated with enhanced excretion of urinary enzymes indicating renal tubular epithelial injury.
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PMID:Acute hyperoxaluria, renal injury and calcium oxalate urolithiasis. 172 37

A new nonionic dimeric contrast medium (CM), iodixanol, was intravenously administered to 40 healthy male volunteers in doses of 0.3-1.2 g of iodine per kilogram of body weight, nonionic monomeric iopamidol and iopentol were administered to 20 others, and the renal effects were studied up to 120 hours after administration. Computed tomography of the kidneys was performed up to 80 hours after injection. Creatinine clearance as an index of the glomerular filtration rate was unchanged with all CM. Urine volume and osmolar clearance increased most with the monomeric CM. The proximal tubular brush border enzyme alkaline phosphatase increased with all CM. The lysosomal enzyme N-acetyl-beta-glucosaminidase increased more with the monomeric CM than with iodixanol. A persistent increased attenuation in the region of the cortex was observed with all CM. Attenuation returned to baseline within 80 hours, with the slowest decline with iodixanol. This delayed cortical enhancement did not correlate with the effects of the CM on the tubular enzyme excretion.
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PMID:Evaluation of renal function with delayed CT after injection of nonionic monomeric and dimeric contrast media in healthy volunteers. 173 60

Renal effects of the 2 non-ionic contrast media iopentol and iohexol were investigated and compared in a double-blind, randomized parallel study where 30 patients received iopentol, and 31 patients iohexol intravenously for abdominal CT. The dosage of contrast medium (350 mg I/ml) was 700 mg I/kg body weight. Only one patient (in the iohexol group) had an increase in serum creatinine of more than 50%. Iopentol and iohexol had no effects on the mean serum values of creatinine, urea, and beta 2-microglobulin (beta 2-MG) nor on creatinine clearance. The urinary excretion of albumin and beta 2-MG was also unchanged. The excretion of the proximal tubular enzymes alkaline phosphatase and N-acetyl-beta-glucosaminidase was increased. No significant difference between iopentol and iohexol was found.
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PMID:Renal effects of iopentol and iohexol after intravenous injection. 186 5

Excretion of urinary N-acetyl-beta-glucosaminidase (NAG), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and gamma-glutamyltransferase (gamma-GT) was studied following single intravenous administrations of a non-ionic monomeric contrast medium (iohexol) at doses of 5.0, 7.5, 10.0 and 12.5 g iodine/kg body wt in rats. Measurements of urinary enzymes, serum urea nitrogen and serum creatinine were carried out on the 2nd, 3rd, 4th and 8th days after treatment. Histological examinations of kidneys were performed on days 3 and 8. From 5.0 g iodine/kg onwards urinary NAG showed a dose-dependent and significant (multiple comparison, alpha = 0.05) increase in the first 18-h urine samples after application. A significant increase in urinary LDH could be observed only at the highest dose of 12.5 g iodine/kg. All other biochemical parameters showed no differences when compared to the control group. The dose-dependent increase in lysosomal NAG correlated with the histological findings, i.e. there was dose-dependent vacuolization of proximal tubular cells, so-called 'osmotic nephrosis'.
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PMID:The use of urinary N-acetyl-beta-D-glucosaminidase (NAG) for the detection of contrast-media-induced 'osmotic nephrosis' in rats. 196 1

Renal toxicity was assessed in 19 patients receiving methyl acetylenic putrescine (MAP), an irreversible inhibitor of ornithine decarboxylase. Patients received 250 mg t.d.s. for up to 13 weeks. This dose effectively inhibited the target enzyme, as shown by elevations in decarboxylated S-adenosyl methionine levels. No significant nephrotoxicity was observed in these patients as determined by plasma urea, creatinine and creatinine clearance measurements, although minor elevations of the urinary enzymes lactate dehydrogenase, N-acetyl-beta-glucosaminidase, alkaline phosphatase and alanine aminopeptidase were observed. As this could represent sub-clinical renal damage, caution should be exercised when using MAP in combination with other cytotoxic drugs.
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PMID:Assessment of renal toxicity by urinary enzymes in patients receiving chemotherapy with 8-methyl-8-acetylenic-putrescine. 196 73

Twelve consecutive patients with a solitary functioning kidney were treated for renal stone by extracorporeal shock wave lithotripsy (ESWL*) with the modified Dornier HM3 lithotriptor and studied for 3 days after treatment. Urinary excretion of electrolytes, N-acetyl-beta-glucosaminidase (NAG), alkaline phosphatase, kallikrein, glycosaminoglycans, albumin and beta 2-microglobulin, and clearances of creatinine, inulin and para-aminohippuric acid were determined, as were serum levels of creatinine, urea, beta 2-microglobulin and aldosterone, and plasma renin activity. Urinary flow rate, free water clearance, and urinary excretion of NAG, kallikrein and beta 2-microglobulin were significantly increased 0 to 24 hours after ESWL. The urinary excretions of alkaline phosphatase, albumin and glycosaminoglycans were unchanged. Glomerular filtration rate was significantly decreased and effective renal plasma flow was unchanged. Filtration fraction was stable. Serum lactic dehydrogenase increased significantly after ESWL and remained high through the period of observation. Serum levels of creatinine, beta 2-microglobulin and aldosterone were unaltered. A decrease in plasma renin activity immediately after treatment is explained by the water immersion and the extracellular volume expansion during treatment.
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PMID:Acute changes in renal function following extracorporeal shock wave lithotripsy in patients with a solitary functioning kidney. 198 13

Experimental evidence suggests that the oxidative metabolites 2,3- and 2,5-dihydroxybenzoic acid (DIOH) may be responsible for the nephrotoxicity of salicylic acid (SAL). In the present study, enzymuria in conjunction with glucose (GLU) and protein (PRO) excretion were used as endpoints to compare the relative nephrotoxicity of SAL with 2,3- and 2,5-DIOH. In addition, the effect of age on enzymuria and GLU and PRO excretion following treatment with SAL or 2,3- and 2,5-DIOH was investigated because the elderly are at greater risk for SAL-induced nephrotoxicity. Three and 12-month male Fischer 344 rats were administered either no treatment, vehicle, SAL, 2,3-DIOH, or 2,5-DIOH at 500 mg/kg p.o. in 5 ml/kg corn oil/DMSO (5:1). Effects of these treatments on functional integrity of renal tissue was assessed from 0--72 h after dosing by measurement of urinary creatinine, GLU, and PRO, as well as excretion of proximal and distal tubular renal enzymes. Enzymes measured as indicators of proximal tubular damage were N-acetyl-beta-glucosaminidase (NAG), gamma glutamyltransferase (GGT), alanine aminotransferase (ALT), and alkaline phosphatase (AP), while urinary lactate dehydrogenase (LD) and aspartate aminotransferase (AST) were measured as indicators of distal tubular damage. In comparison to 3-month vehicle-treated rats, 2,3- and 2,5-DIOH caused a significant increase between 0-8 h in excretion of urinary GLU and activities of AST, NAG, and LD, with peak effects occurring between 4-8 h. Toxic effects of either metabolite were not evident beyond 24 h, and toxicity of 2,5-DIOH was significantly greater in comparison to 2,3-DIOH. SAL treatment resulted in similar effects on enzymuria as well as GLU and PRO excretion, but peak effects did not occur until 16-24 h, and often persisted until 72 h after dosing. Maximal enzymuria in response to SAL treatment was significantly greater in 12- vs. 3-month rats for AST, NAG, and LD. In response to 2,3-DIOH treatment, the maximal response was significantly greater in 12- vs. 3-month rats for LD and AST, and for NAG in response to 2,5-DIOH treatment. The results of this study suggest that both 2,3- and 2,5-DIOH are nephrotoxic metabolites of SAL, but implicate 2,5-DIOH as the more potent nephrotoxic metabolite. The relative lack of an age effect for 2,3- and 2,5-DIOH vs. SAL supports the hypothesis [2] that age-related differences in biotransformation of SAL, and not increased tissue sensitivity to 2,3- or 2,5-DIOH, contribute to the age-related increase in susceptibility to SAL-induced nephrotoxicity.
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PMID:Comparative acute nephrotoxicity of salicylic acid, 2,3-dihydroxybenzoic acid, and 2,5-dihydroxybenzoic acid in young and middle aged Fischer 344 rats. 201 54


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