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)

In the determination of urinary 17-hydroxycorticosteroids, the urine is saturated with NaHSO3 after hydrolysis with beta-glucuronidase and then extracted with methylene chloride. Sodium bisfulfite removes almost all non-steroidal impurities in the urines from patients medicated with acetylspiramycin, leucomycin, erythromycin, triacetylolenadomycin, rifampicin and tranquilizers such as chlorpromazine, which interfere with the absorption at 410 nm. in the subsquent Porter-Silber reaction. In order to increase the specificity of a routine method, a procedure conducted by Allen has been often employed: The sum of 370- and 450-nm. absorbances is subtracted from twice absorbance at 410 nm. However, the procedure could not be used in the medicated urines mentioned above, because the spectral absorption curve of these drugs and their metabolites in the Porter-Silber reaction was not a straight but a strongly convex or concave line in the 370-450-nm. range. Using the present method, interference with the Porter-Silber reaction was not found in the urines from patients medicated with chloramphenicol, minocycline, chlordiazepoxide, meprobamate, methyprylon, nitrazepam, synthetic penicillins such as hetacillin, oxacillin and cloxacillin, or cephalosporins such as cephalexin and cephalothin. However, to obtain correct values in urines from patients medicated with spironolactone, it was necessary to subject the urines to treatment with methylene chloride before enzyme hydrolysis.
Am J Clin Pathol 1975 Sep
PMID:The effect of sodium bisulfite on the removal of drugs and their metabolites interfering with the Porter-Silber reaction in the determination of urinary 17-hydroxycorticosteroids. 116 83

Massive doses of methylprednisolone were given to dogs prior to severe, lethal, hemorrhagic shock. An untreated group of dogs subjected to hemorrhagic shock served as controls. No persistent significant differences were seen in cardiac output, mean arterial blood pressure, superior mesenteric artery flow, and survival. Calculated total peripheral resistance tended to be lower in the treated dogs and was significantly lower after reinfusion of shed blood. Pretreatment with methylprednisolone did not prevent plasma elevations of the lysosomal enzymes, cathepsin D and beta-glucuronidase. Stabilization of hepatic lysosomes in treated dogs subjected to hemorrhagic shock was not evident. The results failed to indicate significant salutary effects of methylprednisolone sodium succinate in this lethal hemorrhagic shock model.
Am J Surg 1975 Sep
PMID:Inadequacy of steroids in the treatment of severe hemorrhagic shock. 116 20

In alkali burned rabbit corneas activities of beta-glucuronidase, N-acetyl-beta-D-glucosaminidase and acid beta-galactosidase were studied histochemically in various time intervals after the traumatization. The technic with semipermeable membranes was employed. Within four days after the injury enzyme activities in the traumatized area were almost lacking. The corresponding activities in the unaffected part of the cornea were within the norm. On the 7th day enzyme activities were on an increase (but still subnormal) in the traumatized area. This area was surrounded by a zone of keratocytes with high levels of enzyme activities. This was particularly remarkable in keratocytes subjacent to the epithelium. The activation of all enzymes studied was present in the basal layer of the epithelium and in the endothelium as well. On the 14th day enzyme activities in the traumatized area were nearly restored and on the 32nd day they could not be distinguished from the normal cornea. Beta-galactosidase displayed a relatively maximal increase in the activity of all enzymes investigated.
Histochemistry 1975 Sep 07
PMID:Alkali burns of the rabbit cornea. I. A histochemical study of beta-glucuronidase, beta-galactosidase and N-acetyl-beta-D-glucosaminidase. 119 85

Arachidonic acid metabolism in resident rat alveolar macrophages and in those activated with complete Freund's adjuvant (CFA) was studied. Adult Sprague-Dawley rats were injected with 0.05 ml CFA, and macrophages were harvested 10 days later. Macrophages were labeled overnight with carbon 14-labeled arachidonic acid, washed, and then stimulated with calcium ionophore A23187 (IoA), phorbol myristate acetate (PMA), or zymosan for 30 minutes. Prostaglandins, thromboxane, and leukotrienes were extracted from the medium and analyzed by radioimmunoassay or radio high-pressure liquid chromatography. Cell lipids were analyzed by radio thin-layer chromatography. Medium and cell beta-glucuronidase activity and protein kinase C activity of the membrane fraction were also assayed. We found (1) lower leukotriene B4 (LTB4) production in stimulated resident macrophages when compared with resident macrophages after IoA stimulation--the suppressed LTB4 production was reversed by PMA; (2) unchanged or higher LTB4 production in activated macrophages when compared with resident macrophages after zymosan stimulation; (3) inhibition of zymosan-stimulated LTB4 production by staurosporine, a protein kinase C inhibitor, in both groups; and (4) lower diacylglycerol (DAG) production in activated macrophages when compared with resident macrophages after IoA stimulation, but not after zymosan stimulation. These results suggest that the reduced response of activated macrophages to IoA is due to decreased production of an endogenous protein kinase C activator. This hypothesis was further supported by the observation that protein kinase C activation in response to IoA was lower in activated macrophages than in resident macrophages. In contrast, zymosan stimulation resulted in higher protein kinase C activation in activated macrophages when compared with resident cells. We hypothesize that protein kinase activation is necessary for leukotriene production and that the preserved ability of zymosan to activate PKC via DAG accounts for the high leukotriene production in zymosan-activated macrophages. We also found that stimulated thromboxane production was higher in activated than resident cells, regardless of the stimulus, and that thromboxane production was not affected by staurosporine. Thus alterations of eicosanoid metabolism in immunologically activated macrophages depend on the stimulus used and the type of eicosanoid examined. Furthermore, leukotriene biosynthesis in rat alveolar macrophages may be regulated by protein kinase C.
J Lab Clin Med 1992 Sep
PMID:Production of leukotrienes and thromboxane by resident and activated rat alveolar macrophages: a possible role of protein kinase C. 132 31

The quaternary structure and binding activity of the murine 46-kDa mannose 6-phosphate receptor (46MPR) were studied in semi-intact murine cells that overexpress the murine receptor. Chemical cross-linking studies showed that the murine 46MPR exists in monomer, dimer, and tetramer forms in membranes of overexpressing murine cells. Treatment of permeabilized cells with Mn2+ increased the tetramer form of 46MPR, and this tetramerization was reversed by removal of Mn2+. Thus, the divalent cations affected the distribution of receptor among the three forms, favoring tetramerization at the expense of dimer and monomer. Low temperature (4 degrees C) also increases the fraction present as tetramer. The binding assay results show that Mn2+ is required for the 46MPR to achieve and retain the ability to bind ligand at 37 degrees C but not at 4 degrees C. Preincubation with Mn2+ produced a 3-fold increase in Man-6-P-specific binding of beta-glucuronidase which paralleled the 3-fold increase in tetramer seen during preincubation with Mn2+. The similarity of the effects of addition and removal of Mn2+ on enzyme binding to the effects of Mn2+ on favoring tetramer formation suggests that divalent cation-dependent tetramerization of the 46MPR contributes to the stimulation of ligand binding to the 46MPR by divalent cations.
J Biol Chem 1992 Sep 15
PMID:Divalent cation-dependent stimulation of ligand binding to the 46-kDa mannose 6-phosphate receptor correlates with divalent cation-dependent tetramerization. 132 39

The activities of four lysosomal enzymes and creatinine levels were measured in the plasma and urine of 17 healthy elderly and 7 young adults. Fractional enzyme excretion (FE ENZ) values for beta-hexosaminidase (N-acetylglucosaminidase), alpha-galactosidase, beta-galactosidase and beta-glucuronidase were calculated and compared between the two groups of subjects. FE ENZ was calculated as the ratio of enzyme clearance to creatinine clearance. The FE ENZ values for alpha-galactosidase, beta-galactosidase and beta-glucuronidase between the elderly and young populations were not statistically different; however, relative to the young control group, the FE ENZ value for beta-hexosaminidase was elevated approximately 2-fold in the elderly population (P = 0.06). The mean urinary alpha-galactosidase activity for the elderly population, when expressed on the basis of creatinine, was 50% lower than that of the control group (P = 0.03), whereas the mean urinary beta-hexosaminidase activity for the elderly was significantly higher compared to the control group (P = 0.008). When data for all subjects was analyzed, no correlation was observed between the urinary excretion of beta-hexosaminidase or alpha-galactosidase and glomerular filtration rate. These data indicate that with advancing age there are changes in the tubular secretion or reabsorption of selective lysosomal enzymes, particularly beta-hexosaminidase and alpha-galactosidase. These biochemical changes may provide a means of assessing subtle progressive deterioration of renal function.
Clin Chim Acta 1992 Sep 15
PMID:Comparison of urinary excretion of four lysosomal hydrolases in healthy elderly and young adults. 133 Mar 76

In this study the causes of organ damage after cardiopulmonary bypass were multifactorial. The concentration of the proteolytic enzyme elastase, which was released from activated granulocytes in the milieu of significantly reduced levels of alpha 1-protease inhibitor (p less than 0.01), increased during cardiopulmonary bypass (p less than 0.01). In addition, bypass initiated platelet aggregation, which both altered the eicosanoid metabolism and caused the level of thromboxane A2 to increase and surpass the level of prostaglandin I2. Because thromboxane A2 dominance subsided immediately after cardiopulmonary bypass, the effect of thromboxane A2 (vasoconstriction) on the development of organ damage may have been influential only during bypass. Both during and after bypass, the increase in endothelin excretion (p less than 0.01 to 0.05) was believed to induce a further vasoconstriction in the microvasculature. On completion of the cardiopulmonary bypass, the elevation of the lysosomal enzyme beta-glucuronidase, which is a sensitive indicator of cellular damage, was influenced by the concentrations of elastase (r = 0.8) and endothelin (r = 0.52). As evidenced by leuko-sequestration in the lung after cardiopulmonary bypass, the increase in the alveolar-arterial oxygen tension difference correlated with the elastase concentration (r = 0.68). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase) was affected by the endothelin (r = 0.68, 0.56) and elastase levels (r = 0.58, 0.68), respectively, but not by the ratio of thromboxane B2 to prostaglandin F1 alpha. The elastase level influenced the pulmonary vascular resistance (r = 0.56). However, neither the cardiac index nor the systemic and pulmonary vascular resistances were influenced by the endothelin level and the ratio of thromboxane B2 to prostaglandin F1 alpha.
J Thorac Cardiovasc Surg 1992 Sep
PMID:Evidence of organ damage after cardiopulmonary bypass. The role of elastase and vasoactive mediators. 135 50

We obtained transgenic maize plants by using high-velocity microprojectiles to transfer genes into embryongenic cells. Two selectable genes were used to confer resistance to either chlorsulfuron or phosphinothricin, and genes encoding either E. coli beta-glucuronidase or firefly luciferase were used as markers to provide convenient assays for transformation. When regenerated without selection, only two of the eight transformed embryogenic calli obtained produced transgenic maize plants. With selection, transgenic plants were obtained from three of the other eight calli. One of the two initial lines produced 15 fertile transgenic plants. The progeny of these plants contained and expressed the foreign genes. Luciferase expression could be visualized, in the presence of added luciferin, by overlaying leaf sections with color film.
Biotechnology (N Y) 1990 Sep
PMID:Inheritance and expression of chimeric genes in the progeny of transgenic maize plants. 136 94

1. The effects of oestrogens, testosterone, progesterone and medroxyprogesterone acetate (MPA) on the rate of N-demethylation of ethylmorphine (EM) to norethylmorphine (NEM) were studied in human adult liver microsomes. 2. N-Demethylase activity was found to be inhibited by progesterone and MPA to a similar extent while oestrogens and testosterone had no or negligible effects. 3. These findings prompted us to measure the N-demethylation of EM in relation to serum progesterone concentration in vivo in three groups of volunteers with large physiological differences in their endogenous levels of progesterone, i.e. i) pregnant women, ii) non-pregnant ovulating women and iii) men. 4. The metabolic ratio (MRP) of EM to NEM in plasma 60 min after dosage and the corresponding ratio in urine sampled for 6 h (MRU,1), measured on two occasions 14 days apart were used to reflect intraindividual variation in the rate of N-demethylation. 5. The average difference in MRP and MRU,1 between the two occasions was similar in all groups. However, the variability in MRP between individuals within a group was significantly higher in ovulating women than in men, but this had no relation to the serum concentrations of progesterone or oestradiol. 6. The cumulative 12 h urinary excretion of EM, NEM and morphine (MO) after hydrolysis with beta-glucuronidase was about 46%. There was no difference in the metabolic ratio of EM to NEM and its conjugate(s) in the urine between the luteal and the follicular phases. Our findings suggest that the menstrual cycle does not influence the rate of N-demethylation of EM.
Br J Clin Pharmacol 1992 Sep
PMID:N-demethylation of ethylmorphine in pregnant and non-pregnant women and in men: an evaluation of the effects of sex steroids. 138 49

Dihydrodiol dehydrogenase (DD; EC 1.3.1.20) purified to homogeneity from rat liver cytosol will catalyze the NAD(P)(+)-dependent oxidation of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (B[a]P-diol) to yield benzo[a]pyrene-7,8-dione (BPQ). To verify that BPQ is a metabolite of B[a]P-diol in rat liver, an S100 fraction was supplemented with NAD+ and NADP+, and the formation of BPQ was followed by reverse-phase HPLC. The identity of BPQ was established by co-chromatography with an authentic standard (under different solvent conditions) and by RP-HPLC using a diode-array detector which established that the metabolite shared spectral identity with BPQ. The formation of BPQ in the S100 fraction was blocked by either a competitive inhibitor (indomethacin) or a suicide substrate [1-(4-nitrophenyl)-propen-1-ol] for DD, indicating that BPQ was being formed by this enzyme. To assess the contribution of DD to the metabolism of [3H]B[a]P-diol, subcellular fractions obtained from uninduced rat liver were fortified with co-factors to optimize the activity of enzymes that would compete for this proximate carcinogen. Under these conditions, S100 fractions fortified with NAD+ and NADP+ metabolized 25% of the B[a]P-diol, producing 731 +/- 154 pmol of BPQ. In contrast, rat liver microsomes fortified with an NADPH generating system metabolize 75% of the B[a]P-diol producing 2614 +/- 379 pmoles of benzo[a]pyrene-tetrahydrotetrols. Rat liver homogenates (S10) fortified with either uridine diphosphoglucuronic acid or phosphoadenosine phosphosulfate produced 180 +/- 56 and 95 +/- 31 pmoles of conjugates respectively, which were recovered as B[a]P-diol after treatment of the aqueous phase with either beta-glucuronidase or aryl sulfatase. Of the metabolites analyzed BPQ was formed in the second largest amount. These studies show that in uninduced rat liver DD may play a significant role in the metabolism of B[a]P-diol. The metabolic fate of BPQ remains to be determined.
Carcinogenesis 1992 Sep
PMID:Contribution of dihydrodiol dehydrogenase to the metabolism of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene in fortified rat liver subcellular fractions. 139 42


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