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)

A study was carried out to examine the effects of ingestion of "BON-NARINE" (BN) on mice immune functions. Mice aged 12 weeks were divided into 4 groups. The first group was given BN at 30 mg/kg (BN-30 group), the second group was given BN at 90 mg/kg (BN-90 group), the third group was given zymosan at 50 mg/kg (Zy group) and the fourth group was a control receiving no treatment. The mice of groups BN-30 and BN-90 were given BN p.o. at doses of 30 mg/kg and 90 mg/kg per day for 20 consecutive days, respectively. The mice of group Zy were given zymosan i.p. at a dose of 50 mg/kg per day for 2 consecutive days. The results obtained were as follows: 1) Potentiation of phagocytic function of the reticuloendothelial system, examined by the carbon clearance method, was seen in the BN-30, BN-90 and Zy groups. 2) The glucose consumption of peritoneal macrophages (M phi) increased significantly in the BN-30 and Zy groups, but not in the BN-90 group. 3) Superoxide anion (O2-) production of peritoneal M phi significantly increased in the BN-30 and Zy groups compared with the control group, but an increasing tendency was observed in the BN-90 group. 4) The acid phosphatase (APH), beta-glucuronidase (GLU) and lactate dehydrogenase (LDH) activities of peritoneal M phi increased significantly in the BN-30, BN-90 and Zy groups. 5) The proliferation of splenocytes induced by Con A in the BN-30, BN-90 and Zy groups significantly increased compared with the control group. These results demonstrated that the ingestion of "BON-NARINE" promotes phagocytic activity in the reticuloendothelial system in mice and has a stimulatory effect on M phi because of increases in glucose consumption, O2- production, APH, GLU and LDH activities in the peritoneal M phi of mice. BN also intensified the T-cell function represented by Con A-induced splenocyte proliferation.
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PMID:[Effects of ingestion of "BON-NARINE" on immune functions in mice]. 783 Mar 47

Cefdinir, a new oral 2-amino-5-thiazolyl cephalosporin, inhibited the luminol-amplified chemiluminescence (LACL) response of human neutrophils stimulated by PMA but not opsonized zymosan, in a concentration-dependent but not time-dependent manner. The LACL response to opsonized zymosan in cytochalasin B-treated neutrophils was, however, inhibited by cefdinir. Various cephalosporins, regardless of the presence of a 2-amino-5-thiazolyl moiety, did not significantly alter the neutrophil LACL response triggered by PMA and zymosan. The LACL response induced by the calcium ionophore A23187 and FMLP was also impaired by cefdinir, and this impairment was increased in cytochalasin B-treated neutrophils. Superoxide anion generation by neutrophils, measured in terms of lucigenin-amplified chemiluminescence and cytochrome c reduction, was not altered. Spontaneous and FMLP-induced neutrophil degranulation, assessed by lysozyme and beta-glucuronidase release, were not modified by cefdinir. Furthermore, cefdinir inhibited LACL generation in cell-free systems consisting of H2O2, NaI, and either horseradish peroxidase or a myeloperoxidase-containing neutrophil extract. Orthodianisidine oxidation in these two acellular systems was inhibited by cefdinir. Cefdinir did not alter neutrophil bacterial killing at concentrations that inhibited myeloperoxidase-containing neutrophil extract-dependent reactions induced by soluble stimuli. Taken together, these data strongly suggest that cefdinir directly inhibits the activity of myeloperoxidase-containing neutrophil extract released into the extracellular medium during neutrophil stimulation by soluble mediators, but has no effect on that released into the phagolysosome during phagocytosis. This unusual property of a member of the beta-lactam family could be of interest in modulating the exaggerated inflammatory process often associated with infectious diseases.
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PMID:Cefdinir (CI-983), a new oral amino-2-thiazolyl cephalosporin, inhibits human neutrophil myeloperoxidase in the extracellular medium but not the phagolysosome. 813 56

Superoxide dismutases (SODs) play a key role in the cellular defense against reactive oxygen species. To study the transcriptional regulation at the cellular level, the promoter of the Nicotiana plumbaginifolia cytosolic gene encoding Cu/ZnSOD (SODCc) was fused to the beta-glucuronidase (GUS) reporter gene (gusA) and analyzed in transgenic tobacco plants. The promoter was highly active in vascular bundles of leaves and stems, where it is confined to phloem cells. In flowers, GUS activity was detected in ovules and pollen grains, in pigmented tissues of petals, and in vascular tissue of ovaries and anthers. In response to treatment with the superoxide-generating herbicide paraquat, very strong GUS staining was observed in photosynthetically active cells of leaves and in some epidermal root cells of seedlings. The expression of the SODCc-gusA was also induced in seedlings after heat shock and chilling and after treatment with sulfhydryl antioxidants such as reduced glutathione and cysteine. It is postulated that SODCc expression is directly linked to a cell-specific production of excess superoxide radicals in the cytosol.
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PMID:Developmental and environmental regulation of the Nicotiana plumbaginifolia cytosolic Cu/Zn-superoxide dismutase promoter in transgenic tobacco. 816 60

The in vitro effect of unfractionated heparin and dermatan sulfate, as well as oligo-heparin and oligo-dermatan sulfate, on human PMN function was investigated. Superoxide anion generation in fMLP-stimulated PMN was dose-dependently reduced by heparin and oligo-heparin, while DS and oligo-DS lacked inhibitory activity. FMLP-stimulated PMN adhesion to endothelial cells was reduced to a similar extent by both heparin and oligo-heparin, but not by DS and oligo-DS. On the other hand, none of the compounds affected the adhesion of unstimulated PMN to either IL-1- or PMA-activated endothelial cells. Heparin and oligo-heparin also inhibited the homotypic aggregation of fMLP-stimulated PMN. As reported, coincubation of platelets with fMLP-stimulated PMN resulted in platelet activation, a process mainly mediated by the PMN-derived serine protease cathepsin G. Both heparin and DS, as well as their oligo-derivatives, reduced platelet activation induced by either fMLP-stimulated PMN or purified leukocytic cathepsin G. Finally, besides cathepsin G, also the activity of beta-glucuronidase and lysozyme released by stimulated PMN were reduced by heparin, oligo-heparin and DS. These data support the hypothesis that heparin and other GAGs may exert an antiinflammatory role.
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PMID:Effect of heparin, dermatan sulfate, and related oligo-derivatives on human polymorphonuclear leukocyte functions. 843 35

Superoxide dismutases (SODs; superoxide: superoxide oxidoreductase, EC 1.15.1.1) play a key role in protection against oxygen radicals, and SOD gene expression is highly induced during environmental stress. To determine the conditions of SOD induction, the promoter of the cytosolic copper/zinc SOD (Cu/ZnSODcyt) gene was isolated in Nicotiana plumbaginifolia and fused to the beta-glucuronidase reporter gene. Oxidative stress is likely to alter the cellular redox in favor of the oxidized status. Surprisingly, the expression of the Cu/ZnSODcyt gene is induced by sulfhydryl antioxidants such as reduced glutathione, cysteine, and dithiothreitol, whereas the oxidized forms of glutathione and cysteine have no effect. It is therefore possible that reduced glutathione directly acts as an antioxidant and simultaneously activates the Cu/ZnSODcyt gene during oxidative stress.
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PMID:Redox-activated expression of the cytosolic copper/zinc superoxide dismutase gene in Nicotiana. 846 30

To investigate the effects of musk-1, a glucoprotein component isolated from the water extract of musk, on the release of superoxide anion as well as beta-glucuronidase and lysozyme of rat polymorphonuclear leukocytes activated by fMLP. An in vitro incubation system with rat polymorphonuclear leukocytes was used. Superoxide anion production was determined by cytochrome C reduction. beta-glucuronidase and lysozyme release was quantitated by enzyme reactions in which phenolphthaleinglucuronic acid and micrococcus lysodeikticus were as the substrates, respectively. In comparison with control, musk-1 at final concentrations of 1-100 micrograms/ml can increase superoxide anion production by 23.0%-83.6% and decrease beta-glucuronidase and lysozyme release by 7%-47% and 9%-22%, respectively, in rat polymorphonuclear leukocytes. It is concluded that Musk-1 can significantly affect the functions of rat polymorphonuclear leukocytes. Therefore, inhibition of lysosomal enzyme release might be considered as one of the mechanisms of anti-inflammatory role of musk.
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PMID:[Effects of the glucoprotein component of musk on the functions of rat polymorphonuclear leukocytes activated by fMLP in vitro]. 1045 95

The effects of differing durations of daily exercise on macrophage functions in mice were studied. Male ICR mice aged 4 wk were divided into five groups: a nonexercise group (control) and four exercise groups with differing daily exercise durations of 15--120 min (Exr groups). The exercise applied was 5 days/wk treadmill running at 13 m/min for 12 wk. The potentiation of the phagocytosis function of the reticuloendothelial system and the glucose consumption of peritoneal macrophages in the Exr 30, 60, and 120 groups were significantly higher than those in the control group. Superoxide anion production of peritoneal macrophages in both the absence and the presence of phorbol 12-myristate 13-acetate in the Exr 60 and 120 groups was significantly higher than that in the control group. The acid phosphatase and beta-glucuronidase activities of peritoneal macrophages in the Exr 30, 60, and 120 groups were significantly increased. These results suggest that treadmill running exercise for at least 30 min/day (30--120 min) effectively enhances macrophage functions in mice. These data provide preliminary evidence indicating that chronic exercise-induced increases in phagocytic activity exhibit a dose-dependent relationship with exercise duration.
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PMID:Effects of different durations of exercise on macrophage functions in mice. 1118 84

The present study aimed at assessing the role of histone H1 in activating macrophages. Histone H1, injected intraperitoneally at a dose of 1 mg/kg body weight as multiple regimens weekly, significantly increased the number of peritoneal macrophages post 21 days of injection. The oxidative and non-oxidative activation of peritoneal macrophages by histone H1 was assessed. For the assessment of oxidative activation the levels of superoxide radical and nitric oxide radical were assessed. The oxidative activation was evident from release of significantly high levels of superoxide and nitric oxide radicals liberated by macrophages of animals treated with histone H1 (P < 0.001) than in untreated animals. In addition, the higher activities of superoxide dismutase indicated protective effect of histone H1, to keep away the macrophages from noxious effects of superoxide. The catalase activity was decreased significantly in macrophages of histone H1 treated animals. The levels of reduced glutathione were significantly (P < 0.001) lowered in treated animals, whereas the levels of lipid peroxides generated were non-significant. The non-oxidative activation was assessed from the activities of lysosomal enzymes released and also from cytolysis of NO-insensitive L929 cells. The activities of lysosomal enzymes-acid phosphatase and beta-glucuronidase released were significantly high in treated animals than in untreated animals (P < 0.001). Histone H1 stimulated the cytolysis of macrophages in L929 cells than in untreated animals. These results suggest that histone H1 stimulates macrophages by oxidative and non-oxidative mechanisms, which favor its future therapeutic prospects.
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PMID:Oxidative and non-oxidative activation of murine peritoneal macrophages by histone H1. 1523 95


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