Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental liver injury with different stages was induced to adult female test rats with daily injection of thioacetamide (ThAA). The doses administered intraperitoneally were 50 mg/kg body weight. In the liver sections progressive changes of damage, regeneration and fat substitution were noticed. Kidney sections revealed enhanced glomerular atrophy, particularly in the cortical tubules, provoked in the 3-week traumatization period. The influence of ThAA on female rat blood was assayed using standard biochemical methods. The analyses done were: the percentage of blood obtainable and the serum/blood ratio; the serum alanine transferase; serum alkaline phosphatase; serum creatinine; serum hydroxyproline and serum beta-glucuronidase activity in the acute, subacute, chronic and highly chronic stage of liver injury. The biochemical findings show continuously progressing damages when traumatization proceeds. In the 3-week test period the histological findings processed showed an increase in osteoclastic resorption in the alveolar bone around the occlusally stressed tooth simultaneously with a horizontal bone loss. Some indications of recovering incidents were seen, too. Only in the histological findings was no difference seen in the deterioration between both sexes, contrarily to the biochemical results also discussed in this study.
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PMID:Influence of thioacetamide-provoked liver injury on female rat blood and alveolar bone under stress. 381 21

Serial renal biopsies for glomerular culture, histochemical staining for beta-glucuronidase, electron microscopy (EM) and light microscopy, were used to study macrophage involvement in experimental chronic immune complex (IC) glomerulonephritis (GN) induced in rabbits by daily intravenous injections of bovine serum albumin (BSA). In the 26 animals studied, proliferative GN of variable severity was induced, with mild disease in 5 animals, moderate proliferation in 15 and crescentic GN in 6. Macrophages first appeared in glomerular culture outgrowths during the 2nd and 3rd weeks, coincident with the onset of proteinuria and rising serum creatinine concentration. Large numbers of macrophages (in excess of 20 per glomerulus) were seen by the 5th weeks and persisted to the 9th week. The number of macrophages in outgrowths was not significantly greater in animals with crescentic disease. EM demonstrated macrophages in capillary loops, and in glomeruli with crescents, macrophages could be seen in the urinary space. Histochemical staining for beta-glucuronidase also demonstrated macrophages in the glomerular tuft and in crescents when present. These results indicate that macrophages constitute a considerable proportion of the glomerular hypercellularity seen in chronic IC glomerulonephritis.
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PMID:Involvement of the macrophage in experimental chronic immune complex glomerulonephritis. 621 16

Serum and urinary kallikrein activities were determined from the arginine-esterase activities in various groups of kidney diseases and were compared with urinary beta-glucuronidase excretion, urinary output, urinary protein content and creatinine clearance. Serum arginine-esterase activity was significantly augmented in the active stage of diffuse renal diseases but was not related to the severity of parenchymal damage. The values improved during remission; the enzyme activity in chronic uraemic patient was as low as in the control sera. There was a positive correlation between urinary output and serum arginine-esterase activity, and consequently serum kallikrein might have an enhancing effect on diuresis.
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PMID:Serum and urinary arginine-esterase activity in paediatric kidney diseases. 657 88

To determine the effect of acute myocardial infarction (AMI) on serum and urinary activity of beta-galactosidase and beta-glucuronidase (lysosomal enzymes) 40 patients were studied. Eighteen patients had acute myocardial infarction and 22 were assigned as controls. Three of the 18 patients with acute myocardial infarction died within 5 to 10 days after hospitalization. Although the serum and urinary beta-glucuronidase and serum beta-galactosidase activity was higher in patients with acute myocardial infarction when compared with the control subjects these differences did not achieve statistical significance. However, the mean values of urinary beta-galactosidase in the control and acute MI groups were 158.68 and 333.3 nmol/mg creatinine/hr, respectively (p less than 0.046). These findings indicate that there is a significant increase in the urine beta-galactosidase activity during the early phases of acute myocardial infarction.
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PMID:Serum and urinary beta-galactosidase and beta-glucuronidase activity in patients with acute myocardial infarction. 681 68

Nephrotoxicity was evaluated in 37 patients receiving aminoglycosides by serial urinary measurements of the low-molecular weight protein beta 2-microglobulin (beta 2m) and the proximal tubular enzymes N-acetyl-glucosaminidase and beta-glucuronidase. Clinical nephrotoxicity, with a rise in serum creatinine greater than 20% of the baseline value, was diagnosed in 15 of 30 evaluable patients. The laboratory diagnosis of nephrotoxicity, defined as a two-fold increase in beta 2m, N-acetylglucosaminidase and beta-glucuronidase, was confirmed in 11/15 patients. Additionally, there were 3 patients in whom there was definitive laboratory nephrotoxicity in the absence of a rise in serum creatinine. The laboratory diagnosis of nephrotoxicity could be made 4.1--5.5 days prior to significant elevation in serum creatinine. The data suggest that beta 2m and enzyme studies are predictors of nephrotoxicity.
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PMID:Aminoglycoside nephrotoxicity and its predictability. 702 43

Proteinuria, albuminuria, urinary beta-glucuronidase and serum creatinine were estimated in 182 workers exposed to organic solvents in four shoe factories, as well as 30 workers with past exposure and 80 control subjects. Ambient air concentrations at each workplace were also measured. In most of these samples, the concentration of organic solvents exceeded the ACGIH recommended threshold limit value for the mixture. Total protein excretion was significantly elevated in exposed workers, although none of the workers had abnormal albuminuria or serum creatinine. Four had increased lysozymuria. There was also a simultaneous elevation of beta-glucuronidase. These findings suggest that a mild and presumably reversible tubular lesion, but not glomerular damage, may occur in workers occupationally exposed to C5-C7 hydrocarbon mixtures.
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PMID:Organic solvents and chronic glomerulonephritis: a cross-sectional study with negative findings for aliphatic and alicyclic C5-C7 hydrocarbons. 718 41

A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HPO4 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells. During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g K2HPO4/kg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and beta-glucuronidase were found on cryostat sections. Kidneys fixed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated. Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosomes into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane. The degradation process described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward the end of the experiment. So far, it is not clear whether the tubular basement membrane is synthesized by the tubular cells, by fibroblasts or by both cell types. The presence of basement membrane-like material in tubular epithelial cells and in parietal epithelial cells of the glomerulus favors the view that epithelial cells produce the basement membranes and that increased production of basement membrane-like material is a sign of loss of differentiation.
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PMID:[Potassium hydrogen phosphate induced nephropathy in the dog. I. Pathogenesis of tubular atrophy (author's transl)]. 742 30

The nature of mutagenic burden due to occupational exposure to tobacco flakes and dust was determined among 20 female tobacco processors (TP) and 20 matched controls (C) by testing urinary mutagenicity in the Ames assay. In addition, urinary cotinine was estimated as a marker of tobacco absorption. Workers and controls were sub-divided into those with no tobacco habit (NH) and those habituated to the use of masheri (a pyrolysed form of tobacco) as a dentifrice (MH). Cotinine was not detected in samples from C-NH while the mean urinary cotinine levels in TP-NH and TP-MH were significantly higher than that in C-MH (3.46 +/- 0.95 and 3.57 +/- 0.46 versus 1.80 +/- 0.58 mM/M creatinine; P < 0.02). The majority of the urine samples from C-NH were non-mutagenic in the presence or absence of rat liver S9 while those from C-H were mutagenic to TA98 and TA102 strains upon metabolic activation. On the other hand, direct mutagenicity to TA98, TA100 and TA102 strains respectively was noted in 6/10, 5/10 and 8/10 samples from TP-NH and 7/10, 4/10 and 3/10 samples from TP-M. Generally, beta-glucuronidase treatment reduced or abolished the mutagenic potential of workers' urine samples indicating that glucuronide conjugates may have partially contributed to direct mutagenicity. Experiments using scavengers of reactive oxygen species revealed that direct mutagenicity in TA102 strain was mediated mainly via hydroxyl radicals. The results clearly demonstrate that tobacco processors are exposed to a wide spectrum of mutagens that cause frame-shift, base pair substitution and oxidative damage.
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PMID:Occupational exposure to unburnt bidi tobacco elevates mutagenic burden among tobacco processors. 776 70

The activities of five lysosomal hydrolases--namely beta-glucuronidase, beta-hexosaminidase, beta-galactosidase, alpha-galactosidase, and alpha-mannosidase--were measured in the plasma and urine of children (ages, 7 to 15 years) with sickle cell anemia (n = 11) and controls (n = 11) from Jos, Nigeria. The presence of SS hemoglobin was confirmed by electrophoresis of red cell hemolysates. Albuminuria was absent in all of the patients with sickle cell anemia. The creatinine-indexed urinary activity level (units of enzyme activity/milligrams creatinine) and the fractional enzyme excretion (FEE) value, which is defined as the ratio of enzyme clearance to creatinine clearance, were determined for each of the five lysosomal enzymes and compared between the two groups. The mean FEE values for beta-glucuronidase and alpha-galactosidase in the sickle cell patients were 10- and 3.5-fold lower, respectively, than the corresponding control values, and these differences were statistically significant (p < .03) for both enzymes; however, beta-hexosaminidase, beta-galactosidase, and alpha-mannosidase levels in urine were not different between the two groups. When indexed to creatinine, a comparison of the urinary enzyme levels of control and sickle cell patients showed significant differences for beta-glucuronidase (p < .01) and alpha-galactosidase (p < .05) but not for the other three enzymes. Differences in level of plasma enzyme activity between control and sickle cell patients were not significant, except for alpha-galactosidase (p < .05), which was increased slightly (25%) in the sickle cell group. These data indicate that there may be abnormalities in the metabolism of lysosomal enzymes in the kidneys of patients with sickle cell anemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased urinary excretion of beta-glucuronidase in sickle cell anemia in Nigeria. 777 Jun 45

It is known that urinary excretion of glucaric acid (GA) is an indirect index of hepatic P-450 microenzyme induction. We measured and analyzed urinary excretion of GA and plasma lipids in non-pregnant women, pregnant women and postpartum women. GA was measured by a new method for the inhibition of beta-glucuronidase activity and plasma lipids were measured by routine laboratory methods and we obtained the following results. 1. The concentration of urinary GA was correlated with that of urinary creatinine in pregnant women. 2. The urinary GA and plasma HDL-cholesterol did not change during the first of gestation, but steeply increased in the middle of gestation, and postpartum values were lower than at term. 3. Plasma total lipids, triglycerides, and total cholesterol continuously increased throughout gestation. 4. Plasma free fatty acids and lipid peroxide steeply increased in late in gestation. These results and several reports suggested that the change in GA in pregnant women reflected their own metabolism not fetal or placental metabolism. It seems that grasping and understanding their metabolism can make their disease clear.
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PMID:[Measurement and fluctuation of urinary glucaric acid in pregnant women]. 808 94


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