Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Rats, mice, and hamsters were fed iota-carrageenan incorporated in a fiber-free, purified diet for 30 days, and the activities of a number of cecal microbial enzymes were determined in vitro. Carrageenan treatment produced cecal enlargement in all species, yet significantly decreased the concentration of bacteria per gram of cecal content. Azoreductase, beta-glucosidase, beta-glucuronidase, nitrate reductase, and nitroreductase activities per gram of cecal content were significantly decreased in the rat, although less consistent effects were found in these enzymes in the mouse and hamster. beta-Glucuronidase and nitrate reductase functions were increased per gram of cecal contents in the hamster. The total activity per cecum of certain of these enzymes was modified by the concomitant cecal enlargement, yet total nitroreductase activity was significantly decreased in all three rodent species. iota-Carrageenan significantly decreased the concentration of enterobacteria, staphylococci, streptococci, lactobacilli, facultative anaerobes, and the total microscopic count in the rat cecum, but did not exert any effect on bacterial viability in vitro. Although having no effect on biliary IgA antibody concentration, iota- and kappa- carrageenan when present at 50 g/kg diet increased the agglutination response of the IgA specific for the hindgut microflora.
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PMID:Influence of dietary carrageenans on microbial biotransformation activities in the cecum of rodents and on gastrointestinal immune status in the rat. 404 88

The authors describe a 70-year-old woman with multiple myeloma and adult Fanconi syndrome. A monoclonal protein of IgA heavy-chain class and kappa light-chain class was demonstrable in the serum. Urine immunoelectrophoresis showed the presence of kappa light chains. Bone marrow aspirate showed increased plasma cells with large bundles of pink-staining Auer-rod-like crystals in their cytoplasm. These crystals failed to stain with Sudan black B, peroxidase, esterase, and PAS, but showed strong acid phosphatase and beta-glucuronidase positivity. Ultrastructural studies showed them to have a fibrillar and an unusual cross-striated pattern. Immunofluorescent studies showed strong IgA and kappa activity in the cytoplasm of the tumor cells, but the fluorescence was absent in the region of the crystals, which were identified easily by their negative birefringence. The authors interpret these observations to indicate that the intracytoplasmic crystals in this case are of lysosomal origin.
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PMID:Nature of intracytoplasmic crystalline inclusions in myeloma cells (morphologic, cytochemical, ultrastructural, and immunofluorescent studies). 619 1

The group of aged subjects being 66 to 97 years old was compared with the middle-age group with regard to various immunological and cytochemical indices related to lymphocytes and neutrophils. The aged showed a lowered count and percentage of T cells, increased count and percentage of "non-B, non-T" lymphocytes, increased percentage of B cells. These alterations in the composition of lymphocyte subpopulation were associated with characteristic patterns of damage affecting the enzyme-positive lysosomal apparatus of lymphocytes with regard to acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase. There was a hundredfold smaller number of cells having intact enzyme-positive lysosomes in the aged than in the group of comparison. The changes mentioned above were also associated with the intracellular accumulation of glycogen in lymphocytes, decreased concentration of IgG and IgM in the serum and various changes in IgA concentration. Neutrophils of the aged were fewer in the blood of the aged than in younger subjects. However, an increased activity of myeloperoxidase, alkaline phosphatase, N-acetyl-beta-D-glucosaminidase, and an increased content of glycogen and lipids could be found in these cells. NBT-positive neutrophil numbers in the aged were lowered if the stimulated test was used and if there were no changes of the spontaneous test.
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PMID:Immunological and cytochemical indices of white blood cells in old age. 619 50

The enzyme histochemistry of the cells lining and within the marginal and medullary sinuses of twenty human reactive lymph nodes has been studied. The sinuses contain luminal ('reticular') cells which are strongly positive for certain hydrolytic enzymes, including acid-alpha-naphthyl acetate esterase, acid phosphatase and beta-glucuronidase. In addition, the lining ('littoral') cells on both sides of the medullary sinuses are positive for these enzymes. In contrast, enzyme-containing lining ('littoral') cells of the marginal (subcapsular) sinuses are observed only on the inner aspect of the sinuses, the outer aspect being negative. Alkaline phosphatase is not present in the sinusoidal cells but 5'-nucleotidase is seen in varying amounts. These findings are supported by an ultrastructural study of three of the nodes, using a staining method for esterase activity. The different enzyme histochemical properties of the littoral cells in the marginal and medullary sinuses closely mirrors that observed when, for example, these structures are stained immunohistochemically for IgA or J chain.
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PMID:An enzyme histochemical study of the sinuses of reactive lymph nodes. 632 11

The murine plasma cell line MOPC 315 efficiently targets newly synthesized acid hydrolases to lysosomes in spite of a marked deficiency in the level of the mannose 6-phosphate receptor (Gabel, C., D. Goldberg, and S. Kornfeld, 1983, Proc. Natl. Acad. Sci. USA, 80:775-779). To better understand the routing of lysosomal enzymes in this cell line, pulse-chase experiments were performed with [2-3H]mannose and [35S]methionine followed by immunoprecipitation of beta-glucuronidase and IgA. By 3 h of chase, essentially all of the newly synthesized beta-glucuronidase had undergone proteolytic processing, suggesting that the molecules had reached lysosomes. At this time 30% of the pulse-labeled IgA was still intracellular. The oligosaccharides on the intracellular IgA were of the high mannose-type, while the secreted IgA contained processed, complex-type oligosaccharides. This indicates that the intracellular IgA was still in the endoplasmic reticulum or an early region of the Golgi complex when all of the beta-glucuronidase had reached lysosomes. Therefore, beta-glucuronidase and IgA must exit from the endoplasmic reticulum or the early Golgi complex at different rates, a finding that is inconsistent with bulk phase movement of these proteins from the endoplasmic reticulum to the trans Golgi complex. The addition of the ionophore monensin greatly slows the rate of IgA secretion from MOPC 315 cells and the molecules secreted have incompletely processed oligosaccharides. In contrast, monensin only slightly delays the transport of newly synthesized beta-glucuronidase to lysosomes and causes no significant alteration in the extent of oligosaccharide phosphorylation, a process that appears to occur in the early (cis) Golgi complex. However, the labeled beta-glucuronidase was deficient in sialylated, phosphorylated hybrid oligosaccharides whose biosynthesis requires the action of late stage oligosaccharide processing enzymes assumed to be localized in the trans Golgi complex.
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PMID:Targeting of beta-glucuronidase to lysosomes in mannose 6-phosphate receptor-deficient MOPC 315 cells. 633 Jan 27

The clearance of circulating IgA immune complexes following acute bile duct obstruction was investigated in this study. IgA immune complexes were formed in vitro from MOPC-315, an IgA M-component with anti-dinitrophenyl (DNP) specificity, and 125I-DNP10 bovine serum albumin (BSA). Eighteen hours after laparotomy during which the common bile duct was either identified only or identified and ligated, the IgA immune complexes were injected intravenously. Groups of bile duct-ligated and bile duct-patent rats were also injected intravenously with IgG anti-DNP-125I-DNP10BSA immune complexes and 125I-bovine liver beta-glucuronidase to assess the hepatic clearance of materials not dependent on an intact biliary system. Clearance of IgA immune complexes was delayed after bile duct ligation. Although the clearance of IgA immune complexes was delayed, only 10% of these complexes remained in the circulation at 3 hr. The clearance of IgG immune complexes and beta-glucuronidase was not affected by ligation. These experiments demonstrate the physiologic importance of a patent bile duct in the normal clearance of IgA immune complexes in the rat. The observation that clearance is delayed, but not completely inhibited by bile duct ligation suggests that alternate mechanisms exist for removing IgA immune complexes from the circulation.
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PMID:The effect of bile duct obstruction on the clearance of circulating IgA immune complexes. 669 69

Phospholipids and cholesterol combine with a protein fraction (IgA and an acid polypeptide) in bile to form the bile lipoprotein complex. We wished to determine whether lysosomes participated only on IgA secretion or if their secretory role also involved the lipid components of the bile complex. This aspect was studied with a single acute injection of chloroquine, a lysosomotropic drug. The results show that a nonnegligible quantity of IgA travels through the lysosomes. In addition, phospholipid and cholesterol levels undergo a significant (P less than 0.05) decrease 1 hr after injection before increasing to normal levels. In contrast to the total inhibition of protein secretion (beta-glucuronidase, acid phosphatase), a transitory decrease of the secretion of bile lipids takes place that suggest secretory mechanisms involving organelles other than lysosomes.
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PMID:Influence of acute injection of chloroquine on the biliary secretion of lipids and lysosomal enzyme on rats. 671 51

The effect of giving yogurt supplements to BALB/c mice on the various gut-associated lymphoid cells was studied. Animals were fed for 2, 5, 7 and 10 consecutive days. The different lymphoid cell types were identified and counted by haematoxylin-eosin staining of histological slices. The numbers of cells secreting IgA, IgG and IgM and the numbers of T lymphocytes were determined by direct immunofluorescence. The degree of activation of the intestinal macrophages in the small intestine was assessed by measuring the beta-glucuronidase (EC 3.2.1.31) released into the intestinal fluid, and also by a histochemical method. Throughout the feeding period, there were no histological alterations in the gut, but there was marked cell infiltration, mainly of plasma cells and lymphocytes. The number of macrophages on the small intestine increased significantly after feeding for 2 d, while the beta-glucuronidase activity was only slightly higher that of the controls. After a 7 d feeding period, the number of IgA secreting cells increased, while the values for cells secreting IgM and IgG and for T lymphocytes remained similar to those of the controls. The effect of giving yogurt on lymphoid cells associated with the large intestine was mainly on the numbers of IgA secreting B cells and T lymphocytes, with a marked increase during the whole feeding period in the latter type of cell. Since giving yogurt mainly enhanced the IgA secreting B cells in both small and large intestines, this increase would strengthen the host's defence mechanisms in the intestinal mucosa. Although the number of macrophages was increased, there was no enhancement in their activity, which might have harmed the host by producing an inflammatory response.
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PMID:Effect of yogurt feeding on the small and large intestine associated lymphoid cells in mice. 782 58

In order to simultaneously assess the local humoral immune and polymorphonuclear leukocyte (PMN) responses in periodontal disease, IgG, IgM, and IgA, as well as the PMN lysosomal enzyme beta-glucuronidase (beta G), were examined in gingival crevicular fluid (GCF) from patients with varying degrees of periodontal pathology. Evaluations were made before and after conservative therapy (scaling and root planing). Thirty patients with varying degrees of periodontal pathology, ranging from mild inflammatory gingivitis to moderate periodontitis, were studied. GCF was collected from the mesial surfaces of all teeth. The presence of the 3 immunoglobulin isotypes was determined by enzyme linked immunosorbent assays (ELISA), while total beta G activity in GCF was determined by a fluorometric assay. Clinical parameters were obtained from 6 sites per tooth. Our data indicate that prior to treatment, total beta G activity is strongly related to the severity of periodontal disease as measured by mean probing attachment level (AL; r = 0.89; P < .005), mean probing depth (PD; 4 = 0.89; P < .0005) and percentage of sites exhibiting bleeding on probing (% BOP; r = 0.49; P < .005). Following treatment, no statistically significant relationship of disease severity and beta G is found. The concentrations of IgG and IgM in GCF do not follow a specific pattern when related to disease severity. In contrast, prior to treatment the concentration of IgA is negatively correlated to mean AL (r = -0.54; P < .005), mean PD (r = -0.59; P < .005), and % BOP (r = -0.47, P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoglobulin isotypes in gingival crevicular fluid: possible protective role of IgA. 789 Dec 51

Advances in our understanding of the relationship between the microbial challenge and the host response in periodontal disease have led to the search for pathogenesis-based risk indicators or risk factors for disease progression. This evaluation is based on analysis of non-invasive or minimally invasive samples that allow measurement of the subgingival plaque microflora or the host response in gingival crevicular fluid (GCF), serum, or saliva. Studies conducted by us have indicated that in GCF, persistently elevated levels of beta-glucuronidase (beta G, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodontitis. This finding has been confirmed in a multicenter trial. We have also observed that a statistically significant positive correlation exists between beta G in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variations in the host response to the challenge. Furthermore, beta G levels in GCF were inversely correlated with the IgG serum antibody titer to a panel of periodontal pathogens, suggesting the essentially protective function of the systemic humoral response in periodontal disease. Data in the literature support this concept. In addition, recent studies of the relationship of antibody isotypes in GCF to progression of clinical attachment loss have suggested that IgA in GCF has a protective function. This may relate to the lack of complement activation by IgA. Alternately, the development of IgA antigen-specific responses are T-cell dependent, and reductions in local levels of IgA may indicate a decrease in T-helper cell function. These data have allowed development of strategies for identifying individual risk profiles for patients with periodontal disease based on the host response to the microbial challenge. With identification of these risk indicators/risk factors for active periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this approach to periodontal diagnosis. Improved patient management should result from the incorporation of these tests into clinical practice.
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PMID:Development of a risk profile for periodontal disease: microbial and host response factors. 804 67


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