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

Many clinical abnormalities in atopic eczema have been attributed to an imbalance in autonomic nervous system control, specifically a partial blockade of beta-adrenergic responsiveness. The lysosomal enzyme beta-glucuronidase is released from granulocytes during in vitro incubation with complement-activated zymosan particles. Isoproterenol will inhibit the release of this lysosomal enzyme from the granulocyte and the isoproterenol effect is associated with increased granulocyte cyclic AMP formation. In atopic eczema and asthma, this granulocyte response to isoproterenol is impaired. Histamine also inhibits in vitro zymosan induced release of beta-glucuronidase and this is an H2 histamine effect. In asthma, this H2 histamine response is diminished. In the following study, we found a similar impairment in histamine inhibition of beta-glucuronidase release and formation of granulocyte cAMP in atopic eczema. This defect was found only in granulocytes from patients with active eczema. Thus in active atopic eczema, defects in the pharmacological response of the granulocyte are not limited to beta-adrenergic agonists but include H2 histamine activity.
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PMID:Impaired H2 histamine granulocyte response in active atopic eczema. 22 50

A 21-year old woman using an oral contraceptive, the combination preparation Trigynon containing levonorgestrel (LNG) and ethinyl estradiol (EE), since June 1987 had experienced pain in the groin. In September 1988 she had a single occurrence of bleeding, a sign of lessened effectiveness of the OC. She was treated with 50 mg of minocycline/day as of April 1989, and for inguinal acne conglobata with locally applied clindamycine (10 mg/ml of clindamycine hydrochloride lotion). She switched to another OC, and the next month timely, normal menstruation ensued. A few days later the dose of minocycline was raised to 100 mg/day. Subsequently she had a regular breakthrough bleeding followed by a missed cycle and a positive pregnancy test. There have been several recent reports about the interaction between antibiotics and OCs (breakthrough bleeding and contraceptive failure). Rifampicin and griseofulvin are known to reduce the activity of OCs via induction of liver enzymes. Between 1968-84 there was a total of 62 failures of OCs (15 using OCs with 50 mcg of EE) reported in the UK. The suspected cause was the combined use with antibiotics (70% penicillin and tetracycline). In the Netherlands 6 cases of possible interactions were reported during 1980-86: 2 cases caused by nitrofurantoin and/or trimethoprim, and 1 case by sulfamethoxazol with trimethoprim. The interference of minocycline with the intestinal flora can occur as 34% of it is excreted in feces, and its antibacterial spectrum corresponds to that of tetracycline hydrochloride (reduction of beta-glucuronidase in the feces). The failure of Trigynon cannot be irrefutable ascribed to minocycline as unintended pregnancy also occurs while using OCs without antibiotics. Clindamycine could have also influenced the intestinal flora percutaneously.
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PMID:[Inefficacy of oral contraception during use of minocycline]. 214 63

Isoproterenol (ISO), histamine (HIS), and prostaglandin E1 (PGE1) inhibit the in vitro release of the lysosomal enzyme, beta-glucuronidase, from polymorphonuclear leukocytes (PMN) during incubation with complement-coated zymosan particles. In asthma, this granulocyte response to ISO and HIS is impaired. Using this in vitro cell model to assess granulocyte beta-adrenergic response, we studied 23 patients with chronic obstructive pulmonary disease (COPD). All had long-standing disease and severe obstruction (FEV1 = 37.5% of predicted). The granulocyte response to HIS challenge in patients with COPD was normal when compared to control subjects, in contrast to the response from the asthmatic group. The granulocyte response to ISO challenge in patients with COPD, however, was reduced compared to control subjects, but not to the degree found in the asthmatics. This demonstrated that reduced granulocyte response to ISO is not limited to asthmatics, but can be found as well in other obstructive diseases of the lung.
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PMID:Impaired in vitro beta-adrenergic granulocyte response in chronic obstructive pulmonary disease. 610 43

Many factors will influence the tissue response to catecholamine stimulation. Isolated human granulocytes (PMNs) release the lysosomal enzyme beta-glucuronidase following incubation with complement-activated zymosan particles. Isoproterenol, histamine, and prostaglandin E1 (PGE1) inhibit this PMN release of beta-glucuronidase. The effect of exercise on this in vitro granulocyte response was studied in two groups: highly conditioned marathon runners (n = 6) and unconditioned subjects (n = 7). A 13-km run did not produce leukocytosis in the highly conditioned marathon runners and the granulocyte response to isoproterenol was unchanged in cells obtained immediately following the run. In contrast, the seven unconditioned subjects exercised to a maximal response on the treadmill. Following exercise there was an increase in plasma catecholamines, a significant leukocytosis, and granulocytes from the immediate postexercise period responded less well to isoproterenol.
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PMID:The effect of exercise on the granulocyte response to isoproterenol in the trained athlete and unconditioned individual. 737 54

The effect of curcumin on lysosomal hydrolases in serum and heart was studied by determining the activities of beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin B, cathepsin D, and acid phosphatase. Rats treated with isoproterenol (30 mg/100 g body weight) showed a significant increase in serum lysosomal hydrolase activities, which were found to decrease after curcumin treatment. Isoproterenol administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin D in mitochondrial, lysosomal, and microsomal fractions. Curcumin treatment returned the activity levels almost to normal, showing that curcumin restored the normal function of the membrane. Histopathological studies of the infarcted rat heart also showed a decreased degree of necrosis after curcumin treatment.
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PMID:Effect of curcumin on certain lysosomal hydrolases in isoproterenol-induced myocardial infarction in rats. 853 67

The effect of growth regulators and culture conditions on the morphogenetic response of cotyledonary leaf discs was studied in popular cucumber variety (Cucumis sativus cv. Sheetal). Organogenesis was induced directly without any intervening callus phase on Murashige and Skoog medium supplemented with different concentrations of benzyladenine and indole propionic acid. Best results (93%) were obtained in the presence of the 4 mg/L benzyladenine and 1 mg/L IPA. The elongated shoots were rooted in basal medium with 1 mg/L indole butyric acid, hardened and transferred to the field conditions. Genetic transformation system has been established for Cucumis sativus cv. Sheetal, plants by infecting cotyledonary explants with Agrobacterium tumefaciens strain LBA4404 carrying binary plasmid pBI121, which contains scorable marker, beta-glucuronidase and selectable marker nptII under the CaMV 35S promoter. Infection was most effective when explants were infected with Agrobacterium for 15 min and co-cultivated for 2 days in the co-cultivation medium. Shoots were regenerated directly from cotyledonary leaf explants in the presence of kanamycin (50 microg/ml) and analysed. Southern blot analysis confirmed that transformation had occurred. This method will allow genetic improvement of this crop by the introduction of agronomically important genes.
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PMID:In vitro organogenesis and genetic transformation in popular Cucumis sativus L. through Agrobacterium tumefaciens. 1263 5

The synergistic effect of nicorandil (K(ATP) channel opener) and amlodipine (calcium channel blocker) on lysosomal hydrolases in serum and heart was examined by determining the activity of beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-D and acid phosphatase on isoproterenol-induced myocardial infarction in rats. The rats given isoproterenol (150 mg kg(-1) daily, i.p.) for 2 d showed significant increase in serum and heart lysosomal hydrolases activity. Isoproterenol administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin-D and beta-glucuronidase in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with nicorandil (2.5 mg kg(-1) daily, p.o.) and amlodipine (5.0 mg kg(-1) daily, p.o.) for 3 d significantly prevented these alterations and restored the enzyme activity to near normal. These findings demonstrate that the pretreatment with nicorandil and amlodipine could preserve lysosomal integrity and hence establish the cardioprotective effect of the combination.
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PMID:Synergistic effect of nicorandil and amlodipine on lysosomal hydrolases during experimental myocardial infarction in rats. 1449 79

The antioxidant activity and the membrane effects of linear furanocoumarin marmesinin isolated from Aegle marmelose was evaluated during experimental myocardial injury. Isoproterenol (150 mg kg(-1) intraperitonially twice at an interval of 24 h) caused increase in the levels of serum marker enzymes via creatinekinase (CK), creatinekinase-MB (CK-MB) isoenzyme, lactatedehydrogenase (LDH) and lactatedehydrogenase isoenzyme (LDH1). It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Marmesinin at a dose of 200 mg kg(-1), when administered orally, demonstrated a decrease in serum enzyme levels and restored the electrocardiographic changes towards normalcy. Myocardial injury was accompanied by the disintegration of lipidperoxides and the impairment of natural scavengers. Marmesinin oral treatment for 2 days before and during isoproterenol administration decreased the effect of lipidperoxidation. It was also shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from the subcellular fractions. Thus, linear furanocoumarin marmesinin could have the protective effect against the damage caused by experimental myocardial injury.
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PMID:Linear furanocoumarin protects rat myocardium against lipidperoxidation and membrane damage during experimental myocardial injury. 1527 22

This study was aimed to evaluate the preventive effect of gallic acid on lysosomal enzymes in isoproterenol treated myocardial infarcted rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of creatine kinase-MB and lactate dehydrogenase were increased significantly (P<0.05) in the serum of isoproterenol induced cardiotoxic rats. The levels of lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides) were significantly (P<0.05) increased and the level of reduced glutathione was significantly (P<0.05) decreased in the plasma and heart of isoproterenol induced cardiotoxic rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D) were increased significantly (P<0.05) in the serum and heart of isoproterenol induced cardiotoxic rats. Isoproterenol induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in lysosomal fraction. Pretreatment with gallic acid (15 mg/kg) to isoproterenol treated rats significantly (P<0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes. Oral treatment with gallic acid (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study show that gallic acid prevents the lysosomal membrane damage against isoproterenol induced cardiac damage and brought back the activities of lysosomal enzymes to near normal levels. The observed effects of gallic acid are due to antilipoperoxidative and antioxidant effects.
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PMID:Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats. 1945 May 77