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)

Neutrophils were preincubated with 17 beta-estradiol and progesterone to determine the effects of these hormones on chemotactic peptide-stimulated superoxide anion (O2-) generation and degranulation. At pharmacologic levels 17 beta-estradiol was more active than progesterone with respect to inhibition of O2- generation as well as degranulation. An increase of preincubation time from 5 minutes to 25 minutes increased the percent inhibition. When 17 beta-estradiol and progesterone were combined at levels which approximate those measured during gestation, there was small but significant inhibition of O2- generation. Dexamethasone at equal molar concentration inhibited O2- generation only after 25 minutes of preincubation and at no time reached the level of inhibition attained by either of the sex hormones alone. Both estradiol and progesterone at pharmacologic levels significantly inhibited beta-glucuronidase and lysozyme release, whereas dexamethasone did not inhibit degranulation despite prolonged preincubation. Neutrophils isolated from women during various phases of the menstrual cycle and during the third trimester of pregnancy did not differ with respect to chemotactic peptide-stimulated O2- generation. These data suggest that inhibition of neutrophil responses requires the continuous presence of pharmacologic levels of estradiol and progesterone.
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PMID:Female hormones reduce neutrophil responsiveness in vitro. 632 34

Using a quantitative cytochemical technique for measuring beta-glucuronidase activity in the peripheral nerves of mice, we have investigated the effectiveness of four potential adjuncts for reducing the dose limiting neurotoxicity of misonidazole (MISO) in the clinic. Under the conditions used, the most effective adjunct was the steroid anti-inflammatory agent dexamethasone. When given over the week previous to MISO treatment, this agent almost completely eliminated the MISO neurotoxicity as determined at week 4 after commencement of MISO dosing. The second most effective adjunct was phenytoin, the third flurbiprofen and the last adjunct, phenobarbitone, was ineffective. Dexamethasone, phenytoin and phenobarbitone all reduced the clearance half-life of MISO and hence the drug exposure dose calculated as the area under the curve of MISO tissue concentration against time. However, no correlation was evident with these parameters and MISO neurotoxicity in the mouse. Dexamethasone, whilst affording protection against MISO toxicity, did not alter the radiosensitivity of the anaplastic MT tumour.
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PMID:The effect of phenytoin, phenobarbitone, dexamethasone and flurbiprofen on misonidazole neurotoxicity in mice. 669 21

The reaction of FMLP with granulocytes causes aggregation and degranulation and enhances adherence to endothelium. To evaluate whether prevention of granule extrusion could impair these granulocyte activities, granulocytes were treated with either dexamethasone or hydrocortisone prior to treatment with FMLP. Dexamethasone was added to suspensions of cytochalasin B-treated granulocytes; it markedly impaired the aggregation response of the granulocytes of FMLP. When cytochalasin-B was not used, granulocyte aggregation in response to FMLP or PMA was inhibited by dexamethasone. Although dexamethasone prevented aggregation of cells following stimulation with FMLP or PMA, it failed to prevent the aggregation of granulocytes induced by rabbit lactoferrin. Adherence of granulocytes to human endothelial monolayers was enhanced by FMLP; dexamethasone inhibited the enhancement. However, with the addition of human lactoferrin to the granulocytes exposed to dexamethasone, the cells were able to adhere as well to endothelium as the cells exposed to FMLP but free of dexamethasone. When cytochalasin-B-treated granulocytes were incubated with dexamethasone or hydrocortisone prior to the addition of FMLP, the subsequent release of lactoferrin was substantially blocked, whereas the release of the primary granule products, lysozyme and beta-glucuronidase, was attenuated but not completely blocked. Thus, corticosteroids might block chemotactic-factor-induced granulocyte aggregation by selectively preventing release of specific granule products that contribute to and sustain aggregation.
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PMID:Mechanism of dexamethasone inhibition of chemotactic factor induced granulocyte aggregation. 705 39

Glucocorticoids have been used in the treatment of a number of diseases where immunological intolerance plays a predominant role. Since immunological intolerance points to the involvement of lysosomal enzymes and glucocorticoids are known to affect their activities, we have attempted to study the effect of these steroids on cardiac and renal enzymes. Dexamethasone, a glucocorticoid, is administered subcutaneously to male Wistar rats at a dosage of 2.5 mg/kg/week on alternate days for two weeks. After withdrawing the steroid, the animals are monitored for one week to oversee the recovery process. Total and free activities of glycohydrolases and cathepsins in serum, heart and kidney are assayed on the days 4, 8, 12, 16 of dexamethasone administration and also on days 4 and 8 following discontinuation of the steroid. During dexamethasone administration, a significant decrease in both the free and total activities of beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, alpha-galactosidase, alpha-mannosidase, cathepsin B and cathepsin D are observed in heart and kidney, but the enzyme levels are shown to increase in serum. On withdrawal of the steroid, the activities of beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase are found to be increased in heart and kidney, whereas, the activity of alpha-mannosidase remains within normal values. Thus, it could be seen that dexamethasone alters the pattern of glycohydrolases and cathepsins, which are involved in protein degradation.
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PMID:Alterations in certain lysosomal glycohydrolases and cathepsins in rats on dexamethasone administration. 871 30