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)

Endotoxin plays an important role in the pathogenesis of septicaemia by activation of cellular and plasmatic systems. This study was performed to investigate the effects of infusion of endotoxin in rabbits by measuring the activation of cellular and plasma systems. Endotoxin was infused at a rate of 1 mg/kg body wt for 10 min, which caused death of all rabbits within 72 h. Endotoxin induced early leukopenia and thrombopenia, increased plasma levels of beta-glucuronidase and leukotriene B4 (LTB4), and decreased complement total hemolytic activity (CH50) and tissue plasminogen activator (t-PA) activity. These observations correlate with the cellular and plasma changes that have been documented in severely ill endotoxemic patients. Therefore, we conclude that this endotoxin model in rabbits is a valuable tool for investigation of pathophysiology and treatment of endotoxic shock.
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PMID:Activation of plasma systems and blood cells by endotoxin in rabbits. 164 34

Endotoxemia in patients can lead to sepsis and shock by activation of cellular and plasmatic systems. Corticosteroids are described to have a beneficial effect on these phenomena. In this study of controlled endotoxic shock, we investigated the protective effects of prophylactic corticosteroid treatment against activation of cellular and plasmatic systems. In this respect, a low-dose methylprednisolone (1 mg/kg body wt) treatment was compared with that of a high-dose methylprednisolone (40 mg/kg body wt) treatment. Endotoxin infusion induced death of all rabbits, which was associated with leukopenia, thrombopenia, increased levels of beta-glucuronidase, and leukotriene B4 (LTB4) and decreased levels of complement total hemolytic activity (CH50) and tissue plasminogen activator (t-PA) activity. Both methylprednisolone regimens prevented death of the rabbits after endotoxin infusion, which correlated with a significant decrease of the granulocyte release product beta-glucuronidase (P less than 0.01). The early leukopenia and thrombopenia were not prevented; however, both cell numbers returned more rapidly to baseline values than in the placebo group (P less than 0.01, P less than 0.05). The LTB4 and CH50 concentration and t-PA activity did not differ significantly between the treated and placebo groups. These results indicate that although methylprednisolone has no inhibitory effect on the activation of the complement, arachidonic acid, and fibrinolytic systems, it protected the animals from the deleterious effects of endotoxin shock by inhibition of leukocyte activation. In this regard a low dosage of methylprednisolone is equally effective as the most often recommended high dose.
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PMID:Methylprednisolone prophylaxis protects against endotoxin-induced death in rabbits. 164 35

The effects of nafazatrom on leukocyte function in vitro and in vivo were related to its ability to salvage ischemic myocardium in an occlusion-reperfusion model of myocardial injury in the anesthetized dog. Nafazatrom (0.4-75 microM) produced dose-related inhibition in vitro of neutrophil aggregation, superoxide anion generation, arachidonic acid metabolism, and, to a lesser extent, the release of beta-glucuronidase. In contrast, nafazatrom (0.4-37.5 microM) did not substantially influence platelet aggregation or the platelet metabolism of arachidonic acid. In vivo nafazatrom (10 mg/kg, po) reduced infarct size from 58 +/- 3% of the risk area (mean +/- SEM, n = 9) in control dogs to 23 +/- 2% of the risk area (n = 9, P less than 0.01). Nafazatrom also reduced the incidence of accompanying arrhythmias. Nafazatrom-induced myocardial salvage was not associated with any hemodynamic changes; moreover, it was independent of platelets, since thrombocytopenia did not prevent nafazatrom from exerting a protective effect. Measurements of the neutrophil-specific myeloperoxidase enzyme in ischemic myocardium indicate that the smaller infarct size in dogs treated with nafazatrom is accompanied by diminished leukocyte infiltration. Thus, the ability of nafazatrom to inhibit neutrophil function in vitro and cell infiltration in vivo may underly its myocardial-protective effects.
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PMID:Nafazatrom-induced salvage of ischemic myocardium in anesthetized dogs is mediated through inhibition of neutrophil function. 298 18

In the work presented here we paid our attention to studying changes of the activity of two lysosomal enzymes-acid phosphatase and beta-glucuronidase in platelets after whole-body irradiation and application of certain clinically applied antifibrinolytics (Antilysin Spofa and epsilon-aminocaproic acid) on the activity of these enzymes in isolated platelets. From the results it is obvious that the activity of acid phosphatase and beta-glucuronidase increases in platelets of irradiated rats with a maximum on the 11th day after irradiation. In the same time interval after irradiation the most remarkable thrombocytopenia was observed. The application of Antilysin or EACA to intact, non-irradiated rats affects remarkably neither the activity of the followed enzymes nor the count of platelets. A statistically significant thrombocytopenia, in a comparison with controls was found in whole-body irradiated rats who received EACA or Antilysin. The postirradiation increase of the level of acid phosphatase in platelets exerts a similar character in rats who received EACA or Antilysin as in those who were only irradiated with a difference that the increase of the level of this enzyme was essentially lower in all the time intervals of interest. The beta-glucuronidase level in platelets of rats, who received EACA, was essentially unchanged as compared to controls. The application of Antilysin altered remarkably the level of beta-glucuronidase in platelets of whole-body irradiated rats in a comparison with a level of this enzyme in platelets of rats who received no Antilysin. Most remarkable changes were observed in latter time intervals (11th and 15th day) when the beta-glucuronidase level in platelets of rats after the application of Antilysin was remarkably higher than that in solely irradiated rats.
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PMID:Changes of the activity of acid phosphatase and beta-glucuronidase in isolated platelets of whole-body irradiated rats. 619 83

Prostaglandins participate in the pathophysiology of endotoxin shock; however, their exact role has not yet been clear. In this study, we investigated the role of the proaggregatory vasoconstrictor, thromboxane A2 (TXA2), an arachidonic acid metabolite, during canine endotoxin shock. The central venous plasma levels of thromboxane B2 (TXB2), the stable metabolite of TXA2, was measured by radioimmunoassay. We also investigated the therapeutic effect of reduced glutathione (GSH), a potential cell-stabilizing sulfhydryl compound, in canine endotoxin shock. Sixty minutes after the intravenous administration of E. coli endotoxin (1 mg/kg), the plasma TXB2 levels were significantly increased from 68.8 +/- 49.0 pg/ml to 318.3 +/- 117.2 pg/ml (N = 5) in the control group and from 67.9 +/- 68,4 pg/ml to 222.6 +/- 133.2 pg/ml (N = 5) in the GSH (300 mg/kg/hr) group. The levels in the GSH group were somewhat lower than in the control group for 60 to 180 minutes after the injection of endotoxin. Thromboxane A2 value appear not to relate to early thrombocytopenia and pulmonary hypertension but to relate to the change of late coagulopathy and of pulmonary vascular resistance. The administration of GSH suppressed the lactic acidemia significantly, however there was a much more decrease in the mean arterial pressure in the GSH group than in the control group. In addition, there was a tendency to inhibit the increase of the serum beta-glucuronidase activity in the GSH group.
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PMID:Thromboxane A2 and hemodynamic-biochemical parameters in canine endotoxin shock. 658 Sep 66

The response of the pony to increasing doses of Escherichia coli endotoxin was evaluated using intravenous and intraperitoneal administration models. Marked changes were seen in all parameters measured following endotoxin administration. Leukopenia (neutropenia, lymphopenia) and thrombocytopenia were not dose-dependent. Similarly, elevated plasma fibrinogen and altered glucose concentrations (hyperglycemia and hypoglycemia), pyrexia and increased lactate/pyruvate ratios were apparent at all endotoxin doses but were not dose related. The widely used packed cell volume and capillary refill time, we well as blood lactate and possibly serum beta-glucuronidase, were increased in a dose-related manner.
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PMID:Dose-response of ponies to parenteral Escherichia coli endotoxin. 702 Aug 94

Thrombocytopenia is a common accompaniment of disseminated histoplasmosis. The yeast form of Histoplasma capsulatum does not directly injure human platelets freed of plasma. Preincubation of H. capsulatum with plasma enabled it to induce prompt platelet aggregation and selective release of [3H]serotonin without release of lysosomal beta-glucuronidase and the cytoplasmic marker, lactate dehydrogenase. Platelet aggregation was mediated by adenosine diphosphate, as shown by the blocking of the reaction by apyrase. Indomethacin inhibited both aggregation and serotonin release, indicating their dependence on prostaglandin synthesis by platelets. Plasma IgG conferred [3H]serotonin-releasing activity after complexing with yeasts, and plasma fibrinogen was necessary for platelet aggregation; classical and alternative complement pathways were not involved. The interaction of H. capsulatum with human platelets, mediated by IgG and fibrinogen without complement, represents a new attribute of this fungal pathogen and may contribute to thrombocytopenia complicating disseminated histoplasmosis.
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PMID:Interaction of Histoplasma capsulatum with human platelets. 740 Jun 26

Recombinant human interleukin-11 (rHu-IL-11) is a multifunctional cytokine with thrombopoietic activity and demonstrated clinical efficacy in treating chemotherapy-induced thrombocytopenia. rHu-IL-11 also exhibits anti-inflammatory activity and is currently in clinical trials for the treatment of several inflammatory diseases. As neutrophils are involved in both innate immunity and an acute inflammatory response, the effect of rHU-IL-11 on the function of human peripheral blood neutrophils in vitro was examined. rHu-IL-11 was not cytotoxic and did not induce superoxide anion production or the release of granular enzymes from resting neutrophils. Phagocytosis and chemotaxis were unaffected. rHu-IL-11 treatment did not block the response of neutrophils to stimulation. Pretreatment with rHu-IL-11 did not reduce production of IL-8 following activation with lipopolysaccharide (LPS) or zymosan A particles. Pretreatment with rHu-IL-11 did not affect the release of lysozyme and beta-glucuronidase in response to A23187 or PMA-stimulated production of superoxide anion. These results indicate that rHu-IL-11 does not directly modulate key functions of neutrophils in vitro.
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PMID:Recombinant human interleukin-11 does not affect functions of purified human neutrophils in vitro. 980 25