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)

1. Lysosome-rich fractions were obtained from foetal liver tissues as early as 35 days uterine age. Foetal lysosomes showed the same ;structure-linked latency' and acid hydrolytic potentiality characteristic of their adult counterparts. 2. The osmotic stability of lysosome-rich fraction from foetal guinea-pig liver tissue was greater than that of the corresponding adult lysosome fractions, p-nitrophenyl-phosphatase being used as marker enzyme. 3. The observation was confirmed by using beta-glycerophosphatase and phenolphthalein beta-glucuronidase as alternative marker enzymes. p-Nitrophenyl phosphate and beta-glycerophosphate appear to act as substrates for the same enzyme. 4. By using p-nitrophenylphosphatase activity measurements it was shown that the osmotic stability of foetal lysosomal fractions decreased with increasing foetal age, but at no time achieved the degree of osmotic instability characteristic of adult lysosomal fractions. 5. The correlation of these findings with the intracellular environment of lysosomes is discussed.
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PMID:The osmotic stability of lysosomes from adult and foetal guinea-pig liver tissue. 430 10

Tumour homogenate fractions, isolated by differential centrifugation, were subfractionated by density-gradient centrifugation. Biochemical and electron microscopic analyses revealed that beta-glucuronidase and cathepsin activity were associated with a class (possibly two) of lysosomal particles of density greater than those of mitochondria and the endoplasmic reticulum. Lysosomes sedimented by low g forces were vacuolar, electron-dense, delineated by a unit membrane and about 0.2mum in diameter. beta-Glucuronidase was also apparently associated with ribosomes whereas cathepsin was bound in part to the endoplasmic reticulum. Catalase and glucose 6-phosphatase possessed slightly different density-gradient sedimentation profiles.
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PMID:The locations of cathepsin activity and beta-glucuronidase in the Guerin T8 tumour. 431 48

Isopycnic equilibration and sedimentation rate studies of rat liver microsomes led previously to the assignment of microsomal constituents into group a1 (monoamine oxidase), group a2 (5'-nucleotidase, alkaline phosphodiesterase I, alkaline phosphatase and cholesterol), group a3 (galactosyltransferase), group b (NADH cytochrome c reductase, NADPH cytochrome c reductase, aminopyrine demethylase, cytochrome b(5) and P 450), and group c (glucose 6-phosphatase, esterase, nucleoside diphosphatase, beta-glucuronidase and glucuronyltransferase). Confirmation and extension of the assignment into groups has been obtained by studying the differential effect of the reagents digitonin, EDTA, and PPi. Digitonin specifically affected the equilibrium density only of the group a2 and (to a lesser extent) group a3, and not of groups b and c under conditions which preserved the structure-linked latency of nucleoside diphosphatase and galactosyltransferase. Within experimental error the rate of sedimentation of all microsomal constituents was unaffected. The morphological appearance under the electron microscope was indistinguishable from that of nondigitonin-treated microsomes, except that a few smooth membranes (< 10%) exhibited broken-looking profiles. Treatment of microsomes with EDTA or PPi detached a substantial part of RNA and released protein in excess over the amount accountable for by detachment of ribosome constituents. This detachment was confirmed by electron microscopy. EDTA and PPi decreased markedly the equilibrium density and the density dispersion of groups b and c, due mainly to the uncoating of rough elements. EDTA and PPi shifted slightly the distribution profiles of groups a towards lower densities, possibly as a result of the release of adsorbed proteins. The combination of EDTA and digitonin, used subsequently, rendered the average equilibrium density of group a2 higher than that of groups b and c. Dense subfractions were thus enriched in constituents of group a2 and showed mainly broken-looking vesicles under the electron microscope. The import of our results on the biochemical and enzymic properties of the subcellular components of the microsome fractions is discussed.
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PMID:Analytical study of microsomes and isolated subcellular membranes from rat liver. IV. Biochemical, physical, and morphological modifications of microsomal components induced by digitonin, EDTA, and pyrophosphate. 436 10

Human blood neutrophilic leukocytes were separated and purified by modifications of the Hypaque/Ficoll and dextran separation methods, resulting in a suspension which was greater than 96% neutrophils. Neutrophils were prepared in 0.34 M sucrose containing heparin and were clarified of nongranular debris by sequential passage through polycarbonate filters of pore size 5 mu and 2 mu. Isopycnic sucrose gradients of such filtrates revealed three major bands. The gradient separated fractions were studied by electron microscopy including peroxidase cytochemistry and by enzyme assay for myeloperoxidase (MPO), beta-glucuronidase, muramidase alkaline phosphatase and acid phosphatase utilizing both p-nitrophenylphosphate (pnp) and beta-glycerophosphate as substrates. Peroxidase-positive granules were observed at both density 1.22 (band A) and density 1.20 (band B). Three peroxidase-negative granules were identified: the round or oval peroxidase-negative granule of density 1.22 (band A) and two smaller granules, distinguishable by size and shape at density 1.18 (band C). Band C granules contain crystalloid inclusions. Peaks of muramidase activity coincided with bands A and C, suggesting the presence of muramidase in the peroxidase-negative granules of density 1.22 and in one or both of the peroxidase-negative granules at density 1.18. beta-Glucuronidase was distributed like MPO, with a major peak in band B and a minor peak in band A. Acid beta-glycerophosphatase was largely in band A. Acid pnp phosphatase was nonspecifically associated with soluble nongranular protein which always remained at the origin of sucrose gradients. Alkaline phosphatase was not granule associated and sedimented alone to density 1.145, which is highly suggestive of a cytoplasmic membrane localization for this enzyme.
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PMID:Separation and characterization of human neutrophil granules. 444 23

Studies on the activity of the glucuronic acid pathway in alloxan diabetic rabbits were carried out. Amount of D-glucaric acid, L-ascorbic acid, and D-glucuronic acid in urine increased in the case of the alloxan diabetic rabbits. The transformation from D-glucuronolactone to D-glucaric acid was higher than normal in the diabetic animals. The expired 14-CO2 decreased and urinary excretion of labeled L-gulonic acid increased after administration of 6-14-C-glucuronolactone in the diabetic rabbits. L-Gulonic acid dehydrogenase, lactonase II, and beta-glucuronidase activities were reduced, and UDPGA-pyrophosphatase, D-glucuronic acid-1-phosphatase, and UDPGA-transferase activities increased in the diabetic rabbit liver. From these results, it may be concluded that an increase of endogenous D-glucuronic acid in the diabetic states could be attributed to a metabolid defect in the step of L-gulonic acid dehydrogenation and to the enhancement of UDPGA-pyrophosphatase and D-glucuronic acid-1-phosphate phosphatase activities.
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PMID:Glucuronic acid pathway in alloxan diabetic rabbits. (I). Urinary excretion of metabolites related to the glucuronic acid pathway. 446 73

The importance of granular (lysosomal) enzymes from neutrophils in producing the tissue damage of acute inflammation has been suggested by much indirect and some direct evidence. This study has investigated the kinetics of release and subsequent fate of granular enzymes from phagocytizing human leukocytes The following observations are made: (a) During phagocytosis, the granular enzyme lysozyme is released from leukocytes into the extracellular medium. (b) Release of lysozyme increases as phagocytic challenge increases, but attains a maximum. (c) Release of lysozyme accompanies phagocytosis and is not a delayed event. (d) The lack of release of a nongranular enzyme, lactic dehydrogenase, indicates that cell damage is not a necessary condition of enzyme release. (e) Like lysozyme, beta-glucuronidase is released from phagocytizing leukocytes. Acid alpha-naphthyl phosphatase and cathepsin also appear to be released, but are not found in appreciable amounts in the extracellular medium, in part because of their lability in solution. These results support the concept that extracellular release of granular enzymes may be a useful secretory function of inflammatory leukocytes which becomes damaging to the host in certain circumstances.
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PMID:The mobilization and extracellular release of granular enzymes from human leukocytes during phagocytosis. 502 60

Three lysosomal-type acid hydrolases were examined in subcellular fractions of the developing epidermis of fetal rats to assess the relationship of degradative enzymes to cornification. As the granular layer developed and cornified between 18 and 20 days (D) of gestation, epidermal acid phosphatase increased, acid phospholipase A remained constant, and beta-glucuronidase activity declined. The enzymes were present in 3,000, 17,000, and 100,000 g particulate fractions and soluble cytoplasm. However distribution differed: acid phosphatase and phospholipase A were more preferentially localized than was glucuronidase in the 17,000 g fraction which excluded mitochondria and ribosomes and was enriched in lamellar granules. The findings suggested that acid phosphatase and phospholipase were present in membrane-bound organelles (e.g., lamellar granules) in the granular layer. Particulate acid phosphatase increased with granular layers on days 19 and 20 while a 7-fold increase in soluble enzyme coincided with cornification on day 20. As shown by isoelectric focusing, the enzyme became more heterogeneous at day 20 than at day 18, suggesting increased glycosylation. The particulate fraction displayed lysosomal characteristics with respect to release of acid phosphatase, which was inhibited by hydrocortisone and enhanced by retinol. When fetal epidermis was allowed to cornify in organ cultures, similar increases in acid phosphatase occurred. The presence of hydrocortisone did not affect increase in total enzyme but a greater proportion remained in the particulate fraction. The findings suggest that particulate acid phosphatase and phospholipase are compartmentalized in organelles with lysosomal characteristics during development of granular cells and that release of phosphatase is coincident with cornification. This may reflect not only exocytosis of lamellar granules but also intracellular release of the hydrolytic enzyme.
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PMID:Acid hydrolases of the epidermis: subcellular localization and relationship to cornification. 618 89

The effect of methylnitrosourea (MNU) on cerebellar and cerebral DNA, RNA, protein, lysosomal enzymes (acid DNase, RNase, phosphatase, and beta-glucuronidase), and 2',3'-cyclic nucleotide 3'-phosphohydrolase (2',3'-CNPase) activities was studied in rats from birth through 12 days of age. Subcutaneous injection of MNU in a dose of 0.625 mmol/kg caused a suppression of increase in weights and content of DNA, RNA, and protein of cerebellum, but no changes in those of the cerebrum or in body weight. Ratios of protein and RNA to DNA were substantially elevated by MNU in the cerebellum but not in the cerebrum. Acid DNase and acid RNase activities of MNU-treated rats were significantly elevated beyond the increase of these activities in controls in the cerebellum, but no change in these activities by MNU was observed in the cerebrum. A slight elevation in acid phosphatase activity was observed in the cerebellum but not in the cerebrum after MNU pretreatment. Beta-glucuronidase and 2',3'-CNPase activities were not changed in the cerebellum or in the cerebrum. These results suggest that in the developing brain, especially in the cerebellum at the mitotic stage, MNU caused cell damage and inhibited cell mitosis.
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PMID:Cytotoxic effects of methylnitrosourea on developing brain. 619 99

T gamma lymphocytes are those lymphocytes that express receptors for both the Fc portion of IgG and sheep erythrocytes. A very high proportion of normal T gamma lymphocytes are large granular lymphocytes (LGL), the cell responsible for most, if not all, natural killer (NK) and antibody-dependent cell-mediated cytotoxicity (ADCC) in humans, rats, and mice. In general, these cells are large lymphocytes with prominent azurophilic granules in the cytoplasm. Recently, a group of lymphoproliferative disorders made up predominantly of T gamma lymphocytes has been described. The most common and best studied of these disorders we refer to as "chronic T gamma-lymphoproliferative disease" (T gamma-LPD). In most cases, this disease represents the abnormal expansion of LGL, which is reflected by an increase in functionally active NK or ADCC effector cells. The chronic T gamma-LPD lymphocytes are generally characterized as E- and EA-rosette positive, acid-phosphatase, and beta-glucuronidase positive and express the pan-T antigens OKT3/Leu-4, OKT11/Leu-5, the suppressor-associated antigens OKT5,8/Leu-2, and the NK-associated antigens Leu-7/HNK-1. Typically, the patients are older, predominantly males and characteristically have a lymphocytosis of predominantly T gamma lymphocytes with lymphocyte infiltration of the bone marrow and often the spleen. While chronic T gamma-LPD is not usually an aggressive disease, the patients are often neutropenic and have recurrent bacterial infections requiring antibiotic therapy. Some patients have benefited from cytotoxic chemotherapy., but most patients have not required chemotherapy. An experimental LGL leukemia in F344 rats appears morphologically, functionally, and clinically similar to the human chronic T gamma-LPD and serves as an experimental model for further examining the ontogeny and function of LGL and may be applicable for exploring new and more effective means for the treatment of patients with chronic T gamma-LPD.
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PMID:T gamma-lymphoproliferative disease and related disorders in humans and experimental animals: a review of the clinical, cellular, and functional characteristics. 623 40

Abnormally low activity of hepatic bilirubin UDP-glucuronosyltransferase was found in 25% of 81 unselected patients with gallstones, as compared with only 3% in 35 controls. At the time of cholecystectomy, the stones were taken for analysis in 48 of 81 patients, and a bile sample was obtained in 42 of them. Among the stones, 75% were cholesterol stones, 15% pigment stones, and 10% 'intermediate' stones. Low hepatic conjugating activity was not preferentially associated with a given type of stone. No relation was found between the enzymic deficiency and the biliary cholesterol saturation index. A high proportion of biliary bilirubin monoglucuronide (over 40%) was found in four of seven patients with low transferase activity, as was earlier demonstrated in patients with overt Gilbert's syndrome. Raised biliary bilirubin monoglucuronide was also found in three patients, out of 46, who had normal transferase but raised biliary beta-glucuronidase activity. There was no evidence that deficient bilirubin conjugation could be a consequence of gallstones: the activity of another hepatic microsomal enzyme, glucose 6-phosphatase, taken as a reference, was measured in 12 patients and was always normal. Taking into account the very high frequency of a bilirubin centre in the cholesterol stones (87% of the cases in the present series), it is suggested that the increased proportion in poorly soluble biliary bilirubin monoglucuronide, which was associated with defective conjugation, could act as a trigger for gallstone initiation, regardless of the final composition of the stone.
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PMID:Possible role of a defect in hepatic bilirubin glucuronidation in the initiation of cholesterol gallstones. 625 64


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