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)

The serum concentrations of FSH, LH, prolactin, testosterone, and estradiol and the enzymatic activities of hyaluronidase, glucosidases (alpha-glucosidase, beta-glucosidase, alpha-mannosidase, N-acetyl-beta-D-glucosaminidase, beta-glucuronidase, and beta-galactosidase), lactate dehydrogenase and its isoenzymes (LDH1, LDH2, LDH3, LDH-X, LDH4), and total proteins were measured in the semen of 69 subjects (8 normozoospermic controls, 7 secretory, and 54 excretory azoospermic subjects). FSH levels rose with the deterioration in spermatogenesis and served to differentiate the secretory from the excretory azoospermias. The only source of hyaluronidase and LDH-X in the ejaculate is the spermatozoa. alpha-Glucosidase activity essentially originates in the epididymis. The seminal determination of alpha-glucosidase and, to a lesser extent, alpha-mannosidase and N-acetyl-beta-D-glucosaminidase helps rapidly, sensitivity, reliably, and noninvasively to differentiate secretory azoospermias (with higher enzymatic activity) from the excretory type (less enzymatic activity) and may be of use in identifying with a certain degree of reliability the site of obstruction in the male genital tract.
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PMID:Enzyme and hormonal markers in the differential diagnosis of human azoospermia. 153 Mar 67

As a basis for studies of the influence of lipids on the immune response and health, adult C57Bl mice were fed for 10 weeks or longer on one of the following diets: high (200 g/kg) polyunsaturated fatty acid, high (200 g/kg) saturated fatty acid and low (50 g/kg) polyunsaturated fatty acid purified diets and a standard commercial diet. The three test-fat diets were compounded to have approximately the same energy content and the mice of each group maintained similar body-weights. High-fat diets significantly reduced their subsequent delayed hypersensitivity response to challenge after sensitization with tuberculin. Immunoglobulin IgM antibody formation against Escherichia coli lipopolysaccharide was transiently decreased, but IgG antibody against sheep erythrocytes and killed salmonella vaccine, IgG and IgE antibodies against ovalbumin remained unaffected. Total and differential blood counts revealed no differences between mice on high-fat and control diets in either the absolute numbers or the proportions of the types of leukocytes. Studies on peritoneal macrophages from mice of each group showed no difference in morphology and they ingested non-toxic and toxic particles releasing similar amounts of lactate dehydrogenase (EC 1.1.1.27) and beta-glucuronidase (EC 3.2.1.31) for each substance, indicating that there were no differences in viability or phagocytic function. The present study shows that the C57 Bl mouse can provide a model for the investigation of some consequence of the reduced immunocompetence induced by high-fat diets.
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PMID:High-fat diets and the immune response of C57Bl mice. 154 99

Acidic sulfate is the most toxicologically important sulfur oxide which exists in the ambient air. To determine if particle size influences toxic effects of sulfuric acid, we investigated the effects of sulfuric acid aerosols of two different sizes on biochemical and cellular parameters of bronchoalveolar lavage fluid from exposed guinea pigs. Guinea pigs were exposed to fine (mass median diameter, 0.3 micron), and ultrafine (mass median diameter, 0.04 micron) sulfuric acid aerosols at 300 micrograms/m3 for 3 hr/day. The animals were euthanized immediately and 24 hr after 1 and 4 days of exposure and lungs were lavaged. Elevated beta-glucuronidase, lactate dehydrogenase activities, and total protein concentration as well as decreased cell viability were observed in the lavage after a single exposure to sulfuric acid aerosols of both sizes. These alterations were small, though statistically significant, and transient. No alteration in these parameters was observed after 4 days of exposure to acid aerosols. In contrast, sulfuric acid-induced alterations in alveolar macrophage function were more pronounced and longer lasting. Immediately after a single exposure to fine acid, there was a 2.7-fold increase in the spontaneous tumor necrosis factor (TNF) release over that in the control group while endotoxin-stimulated TNF release was increased by 2.2-fold. In addition, acid aerosols of both sizes increased the TNF release from macrophages after 4 days of exposure, although there was no clear temporal pattern of induction or recovery. Furthermore, immediately after 4 days of exposure to either fine or ultrafine acid, the amount of H2O2 that could be induced from baseline production by alveolar macrophages was 2.2-fold higher than that of the controls. The phagocytic function of macrophages was also altered by exposure to sulfuric acid aerosols. Twenty-four hours after single or multiple exposure, fine acid enhanced (as high as 78% above control) the in vitro phagocytic activity of alveolar macrophages while ultrafine acid depressed the phagocytic capacity (as much as 50% below that in the control). In addition to these biochemical parameters and cellular functions, we also measured the intracellular pH (pHi) of macrophages harvested after exposures to these acid aerosols using a pH-sensitive fluorescent dye. The resting pHi was depressed after a single exposure to both acid aerosols. The depression in pHi persisted 24 hr after ultrafine acid exposure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of fine and ultrafine sulfuric acid aerosols in guinea pigs: alterations in alveolar macrophage function and intracellular pH. 155 43

Effects of 50% ethanolic extracts from the liver and the gall bladder of Naja naja kaouthia Lesson (COB-L or COB-G) were studied on the phagocytic activity of a mouse reticuloendothelial system. The clearance-rate of carbon was shortened by the oral administration of COB-L or COB-G (50 or 200 mg/kg). COB-L or COB-G promoted the phagocytosis of latex by peritoneal macrophages (M phi). Furthermore, effects of these extracts on the peritoneal M phi were biochemically investigated using in vitro experimental models. The activities of two lysosomal enzymes, acid phosphatase and beta-glucuronidase, and that of lactate dehydrogenase in the peritoneal M phi were enhanced when the M phi were cultured with COB-L or COB-G (10-100 micrograms/ml) for 4 d. In addition, the consumption of glucose in the culture media by the M phi was also enhanced by culturing the media with COB-L or COB-G. When COB-L and COB-G were given orally immediately before and 16 h after the application of picryl chloride (PC) or sheep red blood cell (SRBC), these extracts at a dose of 200 mg/kg did not show any inhibitory effects on the swelling by picryl chloride-inducing contact dermatitis (PC-CD) and by sheep red blood cell delayed type hypersensitivity (SRBC-DTH) in mice. However, these extracts inhibited the immunosuppression with the SRBC 1 x 10(9) cells priming and with the frozen and dried ascites of Ehrlich carcinoma-bearing mice containing immunosupressive substances (EC-sup). These results suggest that COB-L or COB-G biochemically activates the mouse peritoneal M phi, and promotes the phagocytic activity of the M phi and the interaction between M phi and T cell.
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PMID:[Pharmacological study on Naja naja kaouthia Lesson. III. Effects of 50% ethanolic extracts from liver and gall bladder on phagocytic activity of mouse reticuloendothelial system]. 160 42

Female wistar rats were inoculated intratracheally with 10 mg/ml suspensions of various dusts, viz: quartz, fly ash, mica and corundum in physiological saline. Biochemical markers of bronchoalveolar lavage fluid (BALF) were analysed 8 days after the instillation of the dusts. Elevated levels of proteins, sialic acid and phospholipid contents and the activity of lactate dehydrogenase correlated well with the degree of the known fibrogenic potential of different dusts in the lungs in the following order, quartz greater than fly ash greater than mica greater than corundum. beta-glucuronidase activity, was however, only elevated in the quartz inoculated group of rats. It is suggested that biochemical constituents of BALF analysed shortly after the exposure to different dusts can be useful to mirror alterations in the tissue response to mineral dusts.
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PMID:Ranking toxicity of industrial dusts by bronchoalveolar lavage fluid analysis. 160 26

Chloroform hepatotoxicity was investigated in precision-cut liver slices from male Sprague-Dawley rats pretreated with phenobarbital to predispose animals to CHCl3 intoxication. Liver slices were exposed to 0.2, 0.5 and 1.0 mM chloroform for a total of 9 h in a roller culture system. Intracellular K+ loss was found to be concentration- and time-dependent over the duration of the experiment. Histopathological changes were also evident. Glucose 6-phosphate dehydrogenase and beta-glucuronidase were significantly decreased at 3 h relative to controls where a loss of 61% and 36% occurred, respectively. Enzyme levels of alanine aminotransferase and lactate dehydrogenase, both found predominantly in periportal hepatocytes, remained identical to controls over the duration of the experiment. A significant time-dependent depletion of glutathione occurred as early as 3 h following the administration of 0.5 mM chloroform. Mitochondrial viability, measured by the reduction of a specific dye, was significantly lower than controls in treated slices at 6 h following chloroform administration. Precision-cut liver slices appear to be especially useful for the biochemical and histopathological examination of site-specific hepatotoxicants such as CHCl3.
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PMID:The hepatotoxicity of chloroform in precision-cut rat liver slices. 163 1

Stimulation of polymorphonuclear leukocytes with kallikrein demonstrated that enzyme acts selectively on the release of lysosomal enzymes of these cells. The release of collagenase, similarly to the release of lysozyme into the incubation medium increased proportionally to kallikrein concentration and the duration of incubation. Kallikrein had a small effect on beta-glucuronidase secretion. No effect on cytoplasm lactate dehydrogenase release was detected. These results suggest that kallikrein, as a soluble stimulus, predominantly induces degranulation of specific granules containing collagenase capable of degrading the connective tissue. Secretion of lysozyme and collagenase requires the presence of active kallikrein. Soybean trypsin inhibitor diminished the enzyme release.
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PMID:Influence of human plasma kallikrein on lysosomal enzyme release from polymorphonuclear leukocytes. 165 May 20

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


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