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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The capacity of various drugs (acetylsalicylic acid (ASA), ketoprofen, diclofenac, piroxicam, BW 755C, BW A4C, nedocromil sodium and azelastine) to inhibit human polymorphonuclear neutrophil (PMN)-mediated platelet activation was investigated. In this model, stimulated PMN release cathepsin G (Cat G), a serine proteinase which, in turn, induces platelet activation. 2. Among the different tested drugs, azelastine (100 microM for 1 min) was the only one able to prevent platelet aggregation. The cyclo-oxygenase inhibitors were all inactive, although used at effective concentrations as judged by inhibition of thromboxane B2 (TxB2) formation. Inhibition of platelet aggregation by azelastine was concentration-dependent, the range of active concentrations being of 20-70 microM. Release from platelets of 5-hydroxytryptamine was also inhibited at 30 microM and above, but never reached 100%. 3. The inhibition by azelastine is due to an effect on both cells. Indeed, beta-glucuronidase release from activated PMN and platelet activation by purified Cat G were both affected. 4. However, used at high concentrations (greater than 100 microM) azelastine was toxic since it released significant amounts of lactate dehydrogenase (LDH) from PMN and platelets. 5. These results show the capacity of azelastine, an anti-allergic and anti-asthmatic compound, to inhibit the cell-to-cell communication between PMN and platelets, an effect which may be relevant for its therapeutic efficacy or for a new application in diseases in which PMN and platelets are involved.
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PMID:Interference of anti-inflammatory and anti-asthmatic drugs with neutrophil-mediated platelet activation: singularity of azelastine. 165 73

During the procedure of centrifugation cytapheresis donors occasionally experience adverse clinical reactions. We evaluated the possibility of whether activation of granulocytes and their subsequent release reactions, which may have been triggered by this extracorporeal circuit, were responsible for these adverse effects. Six blood samples were obtained during various set intervals during plateletapheresis. Of these, four samples were taken directly from each donor. The remaining two were drawn from the efferent lines, i.e. those which return blood from the cytapheresis machine back to the donor. Reactive oxygen species produced by granulocytes were monitored by chemiluminescence using microamounts of whole blood or isolated granulocytes. Furthermore, secreted granulocyte products such as neutral proteinase elastase, present in plasma in a complex with alpha 1-proteinase inhibitor (complexed elastase), and lysosomal beta-glucuronidase were examined. A complete blood cell count, as well as values of haemoglobin, haematocrit, lactate dehydrogenase, protein, albumin and proteinase inhibitors such as alpha 2-macroglobulin and alpha 1-proteinase inhibitor were also determined. Complexed elastase increased from a preapheresis value of about 140 micrograms/l to about 180 micrograms/l at the end of the cytapheresis. All other clinical chemical and cytological values were 8 to 12 percent lower than preapheresis values, which can be attributed to inherent plasma volume expansion. Reduced chemiluminescence was observed upon stimulation of phagocytes in the whole blood assay (about 700 counts/min x 10(3) x 50,000 cells vs. about 600 counts/min x 10(3) x 50,000 cells). This decrease was also seen with stimulated granulocytes (about 5800 counts/min x 10(3) x 50,000 cells vs. about 4500 counts/min x 10(3) x 50,000 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:On the biocompatibility of IBM 2997 continuous flow plateletapheresis. 170 57

Gingival crevicular fluid was collected from multiple sites in patients with chronic adult periodontitis, and analysed for the lysosomal enzymes beta-glucuronidase and arylsulphatase, the cytoplasmic enzyme lactate dehydrogenase, total IgA, IgG and IgM and the protease inhibitor alpha 2-macroglobulin. The within-mouth (intraclass) correlation coefficients were calculated to describe the relationship between samples collected from individual patients. Data collected at baseline and 3 months after root planing and scaling were analysed, as was the change between examinations. Volume of crevicular fluid demonstrated the smallest intraclass correlation coefficient (0.16 at baseline, 0.12 at 3 months; 0.11 change), while probing depth and enzyme activity had moderate intraclass correlations (i.e. 0.36, 0.36, 0.26 for beta-glucuronidase). Immunoglobulin and alpha 2-macroglobulin activity in the fluid had the strongest correlations (i.e. 0.64, 0.57, 0.65 for IgG). The correlations for anatomically related teeth within a quadrant (molar, non-molar) were equivalent to or greater than the correlation for all samples within a mouth. Examined by tooth type, the intraclass correlations for volume of crevicular fluid, probing depth, beta-glucuronidase, arylsulphatase and lactate dehydrogenase were higher for non-molar teeth. In contrast, intraclass correlations for IgA, IgG, IgM and alpha 2-macroglobulin in samples from molar teeth were either equivalent to or greater than the correlations for non-molar samples. Calculation of intraclass correlation coefficients for such data can (1) indicate the degree of variability present in multiple samples of crevicular fluid collected from individual patients, (2) provide information about the source of host mediators in the fluid, and (3) help identify appropriate sampling strategies for the fluid.
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PMID:Within-mouth correlations for indicators of the host response in gingival crevicular fluid. 170 87

Lipid peroxidation and loss of enzymes located predominantly in either periportal or centrilobular hepatocytes were investigated in precision-cut liver slices from male Sprague-Dawley rats. Pretreatment of animals with 80 mg/kg phenobarbital for the site-specific enzyme studies enhanced and accelerated CCl4 toxicity in slices resulting from increased radical formation. Liver slices were exposed to 0.57 mM CCl4 by vaporization using a roller incubation system at 37 degrees C for a total of 9 hr. Conjugated diene formation, an index of lipid peroxidation, was detected 15 min following CCl4 administration and increased over time. Loss of cytochrome P450 occurred in a time-dependent manner relative to controls where levels in treated slices were 42% of controls at 9 hr. A 48-hr fast prior to termination increased intracellular K+ leakage relative to that present in slices from fed animals. Significant leakage of glucose-6-phosphate dehydrogenase and beta-glucuronidase from centrilobular hepatocytes occurred 9 hr following CCl4 administration. The content of the periportal enzymes (lactate dehydrogenase and sorbitol dehydrogenase) was unchanged in the same slices over the duration of the experiment. Reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide, a mitochondrial selective dye and indicator of viability, was significantly lower in treated slices from phenobarbital-treated animals at 9 hr relative to controls. These studies demonstrate that precision-cut slices are an ideal in vitro system for mechanistic studies and the investigation of site-specific toxicants since the integral architecture of the liver and cellular identity are maintained.
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PMID:Further examination of the selective toxicity of CCl4 in rat liver slices. 173 51

The paper presents experimental asbestosis treated with hydroxy piperquin phosphate (HPQP) in dogs. Results showed that the total cell number of bronchoalveolar lavage fluid, the viability of alveolar macrophages and the enzyme activities of lactate dehydrogenase, acid phosphatase and beta-glucuronidase of alveolar macrophages in treated dogs were higher than those in exposed dogs, asbestos fibers contents in the lungs and the mean scores of lung lesions in the treated dogs were markedly less than those in the exposed dogs. These findings support that HPQP may play a role in protecting alveolar macrophages from damage and inhibiting the progression of lung fibrosis, and that the clinical application of HPQP is somehow evidenced by this study.
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PMID:[Pathological observation of experimental asbestosis treated by hydroxy piperquin phosphate in dogs]. 178 56

One hundred and one young-adult female Sprague-Dawley rats were acclimatized to metabolic cages for 2 days. After that time 24-hour urine was collected at a constant cooling temperature of 0-4 degrees C. After gel filtration the enzyme activities were determined, and the resulting values were used to calculate 24-hour excretions. The following reference ranges (2.5 and 97.5 percentiles) were determined (in mU/24 h): lactate dehydrogenase 43-181; phosphohexoseisomerase 45-1445; glutathione-S-transferase 1-299; alkaline phosphatase 27-1239; leucine arylamidase 72-377; gamma-glutamyltransferase 1334-9188; arylsulphatase A 59-309; beta-galactosidase 76-305; beta-glucuronidase 20-2756; beta-N-acetyl-D-glucosaminidase 66-491; glutamate dehydrogenase 7-711. There was a significant (though not very high) correlation with diuresis for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase, and for glutamate dehydrogenase, lactate dehydrogenase, phosphohexoseisomerase and alkaline phosphatase. The relation to creatinine excretion was markedly close for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase (r = 0.71-0.83), as well as for alkaline phosphatase, leucine arylamidase and gamma-glutamyltransferase. There was a relatively high correlation between the excretion of beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase among themselves (r = 0.63-0.81) as well as between leucine arylamidase and gamma-glutamyltransferase (r = 0.75).
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PMID:Excretion of urinary enzymes in female Sprague-Dawley rats in relation to cellular compartment, creatinine excretion and diuresis. 179 3

The enzymatic profile of urine and plasma in field cases of bovine bladder cancer was studied. Urinary lactate dehydrogenase activity was significantly altered along with the isoenzyme pattern. Activity of alkaline phosphatase and beta-glucuronidase was decreased in the affected animals. No significant changes were observed in acid phosphatase, or arylsulphatase A and B activity. In plasma, lactate dehydrogenase activity was elevated without any change in the isoenzyme pattern. No significant changes were observed in the other plasma enzymes studied or in the sialic acid concentration.
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PMID:The enzymatic profile of urine and plasma in bovine urinary bladder cancer (enzootic bovine haematuria). 180 21

During liver transplantation in the pig, the plasma activities of beta-galactosidase, beta-glucuronidase and beta-glucosidase were elevated as early as 15 min after establishing the hepatic circulation. The enzyme activities peaked at 3 h and returned to the initial level within 2-3 days. However, such substantial alterations were not observed in other enzymes, alpha-mannosidase and alpha-glucosidase. Similar reactions to those of the first three enzymes were found in aspartate aminotransferase and lactate dehydrogenase but with later peaks and slower eliminations. In light of the current study, the serial estimation of acid hydrolases may be useful to discover the extent of tissue injury and also to evaluate the effectiveness of various organ-preservation methods.
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PMID:Plasma lysosomal enzymes after liver transplantation in the pig. 181 48

In utero exposure to di(2-ethylhexyl)phthalate (DEHP; 1000 mg/kg body weight) significantly decreased activities of testicular sorbitol dehydrogenase and acid phosphatase and increased gamma-glutamyl transpeptidase, lactate dehydrogenase and beta-glucuronidase activities at early ages. A decrease in the sperm count of the epididymal spermatozoa was also observed in the sexually matured animals of DEHP exposed group. The data suggest that in utero exposure to DEHP may affect the normal development of testes.
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PMID:Effect of in utero exposure to di(2-ethylhexyl)phthalate on rat testes. 181 82

Testis of male albino rats treated with depot medroxyprogesterone acetate DMPA, at the dose of 1 mg/animal/day for 60 days showed degenerative changes in the late spermatids. The changes were related with the mitochondrial sheath of the midpiece, including the plasma membrane enclosing the mitochondria and the mitochondrial cristae. Except lactate dehydrogenase and alkaline phosphatase, all the testicular marker enzymes, viz. beta-glucuronidase, hyaluronidase, sorbitol dehydrogenase and acid phosphatase registered a significant decrease. The ultrastructural and biochemical changes are correlated, as the cellular degeneration is responsible for decrease in the activity of the marker enzymes.
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PMID:Effect of depot medroxyprogesterone acetate on testis of albino rats: ultrastructural and biochemical studies. 183 39


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