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PubMed1989

Beta-glucuronidase activity in the bile of gallstone patients both with and without duodenal diverticula.

Patients with juxtapapillary duodenal diverticula have an increased occurrence of calcium bilirubinate gallstones. One possible hypothesis to explain this observation is enzymatic deconjugation of bilirubin conjugates in the bile. Beta-glucuronidase of human or bacterial origin may lead to deconjugation of the bilirubin glucuronides in bile. This, in turn, may increase the amounts of unconjugated, water-insoluble bilirubin which can precipitate as calcium bilirubinate, the main component of brown pigment stones. In this study we compared gallstone patients with and without duodenal diverticula treated with endoscopic papillotomy. Increased occurrence of bacteria producing beta-glucuronidase (p less than 0.01) and increased activity of bacterial beta-glucuronidase (pH 7.0) in the bile itself (p less than 0.01) were found in patients with duodenal diverticula. When the activity of the enzyme at pH 4.5, the optimum of the human enzyme, was measured, no such difference was found. The results support the hypothesis of bacterial glucuronidase as an etiologic factor in pigment gallstone disease in patients with duodenal diverticula. The high activity of bacterial enzyme found in the bile in some patients without diverticula suggests bacteria as an etiologic factor, independent of the presence of diverticula.

Aged↗
PubMed1988

Androgen environment and beta-glucuronidase activity in the human kidney.

Basal beta-glucuronidase activity was measured in the cytosol of renal cortex in 10 women and nine men, and its levels were correlated to the concentrations of the main circulating androgens and to the cytoplasmic androgen receptor content. beta-Glucuronidase activity in women was similar to that found in men, despite blood testosterone levels being higher in the latter. The activity of the enzyme does not appear to be related to circulating levels of either testosterone or androstenedione. Only in men the androgen receptor content and dehydroepiandrosterone-sulphate levels were inversely correlated to beta-glucuronidase. In the human kidney cytosol there is no evidence of sexual dimorphism in basal beta-glucuronidase activity; whereas the total testosterone circulating levels do not seem to control the enzyme activity.

Adult↗
PubMed1975

Concerted action of beta-glucuronidase and beta-acetylglucosaminidase on hyaluronodextrins.

A kinetic analysis of the stepwise alternating action of beta-glucuronidase and beta-acetylglucosaminidase on oligosaccharides and dextrins derived from hyaluronic acid was undertaken, for better definition of the contribution of this process to hyaluronate catabolism. Production of monosaccharide from larger dextrins by action of either enzyme is powerfully inhibited by electrolyts. In the study, as in mammalian tissues, beta-glucuronidase is present in excess so that the concentration of beta-acetylglucosaminidase is rate controlling in the action on dextrin substrates. For this action, Vmax shows limited variation with ionic strength or molecular weight of substrate. At ionic strength 0.03, but not 0.18, Km decreases some 100-fold for increase of molecular weight from 2,000 to 15,000. It is specifically this decrease in Km that accounts for the prominent electrolyte inhibition observed with larger dextrins. The extremely low values of Km are attributed to multiple ionic enzyme-substrate interactions at sites remote from the catalytic center. The previously reported stimulation by electrolyte of the action of beta-glucuronidase and beta-acetylglucosaminidase on aryl glycosides, studied briefly, is apparently unrelated to the electrolyte effects seen with dextrins. The catabolic contribution of beta-glucuronidase and beta-acetylglucosaminidase appears to be restricted to hydrolysis of the smaller oligosaccharides produced by action of hyaluronidase, since, for any reasonable assumptions regarding cellular environment, the extent of their action on polymeric hyaluronate or larger dextrins must be limited.

Acetylglucosaminidase↗
PubMed1994

Inhibitory effect of Bifidobacterium longum cultures on the azoxymethane-induced aberrant crypt foci formation and fecal bacterial beta-glucuronidase.

Epidemiologic and experimental studies suggest that consumption of fermented milk products and lactic bacterial cultures that are used to ferment the dairy products, decrease the incidence of certain types of cancer. The present study was designed to determine the effect of lyophilized cultures of Bifidobacterium longum (B. longum), a lactic bacteria, on the azoxymethane (AOM)-induced preneoplastic lesions such as aberrant crypt foci (ACF) formation in the colon and on fecal bacterial beta-glucuronidase activity in male F344 rats. At 5 weeks of age, groups of animals were fed the AIN-76A (control) and the experimental diets containing 1.5% and 3% lyophilized cultures of B. longum. At 10 weeks of age, all animals received sc injection of AOM dissolved in normal saline at a dose rate of 20 mg/kg body wt, once weekly for 2 weeks. The animals were necropsied 6 weeks after the last AOM injection, and the ACF were visualized under light microscopy in the formalin-fixed, unsectioned methylene blue-stained colons where they were distinguished by their increased size, more prominent epithelial cells, and pericryptal space. The cecal contents were analyzed for bacterial beta-glucuronidase activity. The feeding of lyophilized cultures of B. longum significantly inhibited the ACF formation (53%) and the crypt multiplicity in the colon. A significant decrease in the fecal bacterial beta-glucuronidase was also observed in the animals fed the diets containing Bifidobacterium supplements as compared with control diet. These results demonstrate that B. longum in diet influences the metabolic activity of certain types of intestinal microflora that are involved in the production of beta-glucuronidase. Furthermore, the findings also suggest that B. longum supplements inhibit ACF formation, an early preneoplastic marker of malignant potential in the process of colon carcinogenesis.

Animals↗
PubMed2002

Assessment of beta-glucuronidase levels in goat's milk as an indicator of mastitis: comparison with other mastitis detection methods.

The use of somatic cell counts (SCCs) for the diagnosis of mastitis is not a well-established procedure for the caprine species, because nonleucocytic cell-like particles are normally observed as a result of the apocrine secretion process of the goat mammary gland. The infection levels of 124 goats were measured by the beta-glucuronidase test, which was compared with the SCC method and the California mastitis test (CMT). Seventy-nine of 124 samples (63.7%) showed SCCs lower than 1.3 x 10(3) cells per ml. Of these samples, 93% showed low levels of beta-glucuronidase activity (< 15 U/ml). In the remaining 36.3% of the samples, SCCs were higher than 1.3 x 10(3) cells per ml. Of these samples, 88% showed high levels of beta-glucuronidase activity (15 to 100 U/ml). The CMT gave similar results. In this study, the beta-glucuronidase test was standardized for goat milk and shown to be reliable, enabling one to count only the somatic enzyme cells in milk and avoiding the interference encountered with the SCC method.

Animals↗
PubMed1975

B-glucuronidase in duodenal secretions.

Determination of B-glucuronidase activity was carried out in 203 subjects including 60 controls. A modified technic for assaying B-glucuronidase activity was used that employs glass column chromatography and Sephadex. Although the lowest mean value was in the group of patients with cancer of the pancreas, there was wide range of activity of B-glucuronidase in all groups and subgroups and considerable overlap in values between them. It was concluded, therefore, that B-glucuronidase activity assay of the duodenal contents was of no value as a diagnostic test for cancer of the pancreas or for distinguishing between the several diseases affecting the pancreas.

Acute Disease↗
PubMed1992

Beta-glucuronidase and hyperbilirubinemia in breast-fed versus formula-fed babies.

Breast milk and formula milk and the corresponding serum samples from 20 breast-fed babies, 20 formula-fed babies, and their mothers were examined at 3 days of age for beta-glucuronidase enzyme. Serum indirect bilirubin levels were also examined for all the infants. Serum indirect bilirubin concentrations were significantly higher (p < 0.001) in breast-fed (4.87 +/- 2.4 mg/dl) than in formula-fed infants (1.04 +/- 0.5 mg/dl). beta-glucuronidase activity in formula milk was negligible, while that in human milk was considerable (468.26 +/- 220.8 Sigma units/ml) and was correlated (p < 0.05) with that in the serum of the breast-fed (66.13 +/- 18.1 Sigma units/ml) than in formula fed infants (52.08 +/- 11.9 Sigma units/ml) and a significant (p < 0.05) correlation was found between its serum level and serum indirect bilirubin in both breast and formula fed infants. Also in breast-fed infants serum bilirubin concentrations were related to beta-glucuronidase activity in breast milk (p < 0.05): Breast milk beta-glucuronidase--by facilitating intestinal reabsorption of bilirubin--seems to be an important factor in the neonatal hyperbilirubinemia of breast-fed babies.

Bottle Feeding↗
PubMed1991

Alpha-difluoromethylornithine inhibits bone resorption in vitro without decreasing beta-glucuronidase release.

Our previous studies suggested that the ornithine decarboxylase inhibitor alpha-difluoromethylornithine (DFMO) inhibits bone resorption by mechanisms that are independent of polyamine depletion. To determine whether DFMO prevents calcitriol-stimulated bone resorption by acting at a step before or after osteoclast activation, we compared the effects of DFMO on release of calcium and beta-glucuronidase from cultured neonatal mouse calvaria. DFMO, at concentrations of 7.5-20 mM, inhibited release of calcium from calcitriol-stimulated calvaria but failed to inhibit the calcitriol-stimulated increase in beta-glucuronidase secretion. In contrast, ornithine, putrescine, spermidine, and spermine, at concentrations with effects on resorption comparable to those of DFMO, inhibited the effects of calcitriol on both calcium and beta-glucuronidase release. NaF (0.2 mM), like DFMO, inhibited calcitriol-stimulated calcium release without affecting medium beta-glucuronidase activity, whereas elevated phosphate (3 mM) inhibited both activities. The results suggest that DFMO, over the concentration range studied, inhibits calcium release by making the matrix resistant to resorption rather than by acting at a cellular locus.

Animals↗
PubMed1988

Overlapping transcriptional units on the same strand within the murine beta-glucuronidase gene complex.

We have identified and partially characterized a complex transcriptional unit within the murine beta-glucuronidase gene complex on chromosome 5. On the same strand and within the first intron of the beta-glucuronidase structural gene, Gus-s, we observe an RNA polymerase II promoter motif. That sequences within this carefully defined region can promote RNA polymerase II transcription is supported by results of in vitro transcriptional runoff assays and by expression of a linked reporter gene in both cultured cells and transgenic mice. Results of RNA blot hybridization and S1 nuclease protection studies reveal a 2.2-kilobase processed liver transcript which is initiated just downstream of the promoter motif and sharing little, if any, sequence with the 2.7-kilobase beta-glucuronidase mRNA. Both RNA species are found in liver where beta-glucuronidase is known to be expressed in all cell types. To our knowledge, this is the first description of eukaryotic mRNAs from overlapping transcription units which share the same strand yet exhibit little, if any, sequence similarity. A possible regulatory relationship between these overlapping structural genes is discussed.

Animals↗
PubMed1985

[A study of the optimum dose of a glucocorticoid, methylprednisolone sodium succinate, before and after neurosurgical major operations--relationship between beta-glucuronidase level and post operative brain edema].

The effects of pre- and postoperative administration of methylprednisolone (5, 10, 15 mg/kg/day) was studied on 50 cases of major neurosurgical operation. The serum level of beta-glucuronidase was also analyzed in 20 cases so as to determine whether it could be useful as an indicator of post operative brain edema. Methylprednisolone seemed to be effective in the cases administrated in the dosage of 10, 15 mg/kg/day. However, several kinds of postoperative infections were seen in the cases administrated 15 mg/kg/day. The results may suggest that the dosage tested, 10 mg/kg/day, causes little side effects while it is clinically effective. The serum level of beta-glucuronidase tended to increase from the second postoperative day to the seventh day. Those increase were remarkably in the cases with brain edema. Recovery of beta-glucuronidase level was earlier in the cases with 10 mg/kg/day administrated rather than in the cases with 5 mg/kg/day administrated. These results suggest that the measurement of serum beta-glucuronidase level may be useful for evaluating the degree of brain edema.

Adolescent↗
PubMedDate not supplied

[Beta-glucuronidase activity in the gastric juice and gastric mucosa of rats subjected to protein deficiency].

The experiment was performed in order to evaluate the beta-glucuronidase activity in gastric juice and gastric mucosa of rats submitted to protein-free diet. A group of 36 young adult male wistar rats was fed a protein-free diet ad libitum for five weeks; a second group of 36 wistar rats ingested a purified isocaloric 12,5% casein diet for the same period. The concentration of proteins in plasma, gastric juice and gastric glandular mucosa and the beta-glucuronidase activity in the gastric juice and gastric glandular mucosa were determined. Protein deficient rats had lower plasma protein concentration and also a lower protein concentration in gastric juice and gastric mucosa. In these animals there was no significant change of beta-glucuronidase activity in the gastric juice, but there was a significant increase of the specific enzimatic activity in the gastric mucosa. The results suggest that protein restriction in young adult rats affects the gastric mucosa. The increase of the specific beta-glucuronidase activity might be due to heightened local catabolism or to a comparatively more severe protein depletion.

Animals↗
PubMed1984

Cancer-associated alteration of beta-glucuronidase in human lung cancer: elevated activity and increased phosphorylation.

beta-Glucuronidase from human lung neoplasms of various histological types and from uninvolved tissues was studied. A significant elevation of beta-glucuronidase activity was observed in adenocarcinoma and squamous cell carcinoma of the lung as compared with the corresponding uninvolved tissues (P less than 0.01). Saccharo-1,4-lactone, a strong inhibitor of the enzyme, exhibited a substantially greater stabilizing effect on the adenocarcinoma enzyme than on the other enzymes. However, removal of the carbohydrate moiety from the adenocarcinoma enzyme by treatment with endo-beta-N-acetylglucosamidase H (endoglycosidase H) brought about a decrease in the stabilizing effect. Tumor beta-glucuronidase showed considerable negative charge heterogeneity in the pI range from 4.2 to 6.2 in isoelectric focusing on polyacrylamide gel. Upon treatment with exogenous alkaline phosphatase or endoglycosidase H, the heterogenous variant forms of the tumor enzyme appeared to partly or completely lose their negative charge and to be converted into forms similar to those of the normal lung enzyme. These data strongly suggest that the variants are highly phosphorylated on the oligosaccharide chains of the enzyme. An experiment on the labelling of beta-glucuronidase with [32P]-phosphoric acid provided further evidence that the acidic variants found in lung cancers are extensively phosphorylated forms of the enzyme.

Adenocarcinoma↗
PubMed1984

Kinetics of beta-glucuronidase induction by androgen. Genetic variation in the first order rate constant.

Measurements of enzyme activity, rates of protein synthesis, and mRNA activity suggest that the induction of beta-glucuronidase in mouse kidney in response to androgen is regulated at a pretranslational level. Following an initial lag period, the rate and extent of induction follow the rules of simple turnover kinetics and can be described in terms of a zero order rate constant for acquisition of mRNA activity (ka) and a first order rate constant for loss of activity (kb). Genetic variation in kb, described here for the first time, alters the half-time and extent of induction. Variation in kb is independent of previously described variation in ka and, unlike changes in ka, is not associated with change in the lag time. The DNA sequences determining kb, like those determining ka, are genetically linked to the structural gene for beta-glucuronidase. Following the removal of androgen, beta-glucuronidase activity, rate of synthesis, and mRNA activity all decline rapidly with half-lives of 1-2 days. Even in the most rapidly inducing strains, this is significantly faster than the half-time for induction determined by kb. Furthermore, genetic variation in kb does not affect the rate of de-induction. These facts suggest that kb may not describe the turnover of beta-glucuronidase mRNA, but rather the turnover of another step in the induction process.

Animals↗
PubMed1981

[Changes in total beta-glucuronidase activity and DNA content of various tissues and organs of newborn rats after prenatal administration of glucocorticoid].

Quantitative biochemical analyses of the beta-glucuronidase total activity and the total DNA-content carried out on selected parenchymal and mesenchymal organs of 455 Wistar inbred rats (strain Chbb:THOM (SPF) from 56 litters (untreated or treated with 1 mg betamethasone/kg b.w. s.c. on both the 18th and 19th days of pregnancy, applied to the mother animal) led to the following results: The DNA-content of lung, liver, kidney, skin and rib cartilage declined continuously both in the controls and in the treated group during the postnatal observation period (from the 1st to the 15th day p.p.). The prenatal glucocorticoid administration led to a decline in the DNA-content in comparison to the untreated controls, especially evident in the first postnatal days. The beta-glucuronidase activity of lung, liver and kidney showed an increase in the postnatal development phase to a maximum occurring organ-dependently on different days with a decrease afterwards. Due to glucocorticoid-pretreatment of the mother animals the newborn rats showed significantly higher enzyme values within the first postnatal days than did the untreated controls. Between the 6th and 9th day (depending on the organ) the same beta-glucuronidase activities could be found on pretreated and untreated animals. For the further ages tested in this study (till the 15th day of postnatal development) the enzyme activity of the experimentally treated litters was lower than that of the untreated controls. In connection with related findings, especially regarding morphological changes in the lung, the induction of beta-glucuronidase as well as the decrease in the DNA-content due to prenatal glucocorticoid pretreatment are discussed in terms of a maturation acceleration.

Aging↗
PubMed1994

Overexpression rescues the mutant phenotype of L176F mutation causing beta-glucuronidase deficiency mucopolysaccharidosis in two Mennonite siblings.

Two beta-glucuronidase-deficient Mennonite siblings were found to be homozygous for a mutation in exon 3 of the beta-glucuronidase gene that produces a Leu-->Phe substitution (L176F). The siblings also have the previously described benign polymorphism, P649L. Although their cultured fibroblasts contained 1.5-2.2% of normal beta-glucuronidase activity, transient expression of the L176F/P649L cDNA in COS cells produced nearly as much enzyme activity as the wild-type control cDNA. The L176F/P649L enzyme was as stable as wild-type enzyme following endocytosis by fibroblasts and delivery to lysosomes, but was more labile to heat inactivation at 65 degrees C. To study the mutant enzyme at lower levels of expression, we stably transfected mouse mucopolysaccharidosis type VII cells with the L176F/P649L cDNA and selected single-copy cell lines. Metabolic labeling with [35S]methionine revealed that cell lines expressing the mutant enzyme activity at low levels (7-10% of the wild type) actually produced the same amount of enzyme protein as the cell lines expressing the more active wild-type enzyme. However, the cell lines expressing four times this much mutant enzyme protein produced 150-200% as much enzyme activity as the cell line expressing the single-copy wild-type cDNA. These data suggest that overexpression can drive the folding reaction or the self-association of mutant monomers to form active tetramers and, at least partially, correct the beta-glucuronidase deficiency seen at low levels of expression with certain missense mutations.

Alleles↗
PubMed1996

Molecular analysis of patients with beta-glucuronidase deficiency presenting as hydrops fetalis or as early mucopolysaccharidosis VII.

Although not all mucopolysaccharidosis type VII (MPS VII) neonates present with hydrops fetalis or with related symptoms, hydrops fetalis is a common form of presentation of this mucopolysaccharidosis. We used reverse-transcription-PCR-SSCP and direct sequencing to screen for mutations in the human beta-glucuronidase cDNA of 17 MPS VII patients with severe presentation of the disease. Mutations resulting in an unstable mRNA were detected in genomic DNA with direct sequencing of the PCR-amplified beta-glucuronidase exons. We found extensive genetic heterogeneity in MPS VII alleles: in addition to 6 or 12 previously reported mutations (L176F, R216W, R357X, R382C, W507X, and W627C), we detected 14 undescribed mutations in the beta-glucuronidase coding region that produce MPS VII alleles (G136R, E150K, S312X, Y320S, Y320C, H351Y, R382H, R374C, R435P, R477W, G572D, Y508C, K606N and 1900 delta GA). The mutations in hydropic fetuses were widely scattered in the beta-glucuronidase gene. Analysis of three polymorphic sites of the mutant alleles (1766T/C, 1972C/T and a new 1091+27C/G polymorphism) allowed exclusion of identity by descent for some recurrent mutations. Three of four mutations introducing a premature translation stop codon were found to affect mRNA abundance and/or structure. Expression studies provided evidence for the causal relationship between each of the mutations found in MPS VII alleles and the enzyme deficiency, in that all mutations identified exhibited markedly reduced enzyme activity expressed in COS7 cells following transfection with the mutant cDNA.

Adult↗
PubMed1996

Involvement of beta-glucuronidase in intestinal microflora in the intestinal toxicity of the antitumor camptothecin derivative irinotecan hydrochloride (CPT-11) in rats.

Irinotecan hydrochloride (CPT-11), an antitumor camptothecin derivative, causes severe forms of diarrhea clinically. We characterized CPT-11-induced diarrhea histologically and enzymologically and assessed the relationships between intestinal toxicity and the activity of the enzymes that play a key role in the major metabolic pathway of CPT-11 in rats. CPT-11 (60 mg/kg i.v. for 4 days) induced intestinal toxicity characterized by severe chronic diarrhea, loss of body weight, and anorexia. Histological damage was most severe in the cecum. The segmental difference in the degree of the damage showed good correlation with the beta-glucuronidase activity in the contents of the lumen in each case, but not with the intestinal tissue carboxylesterase activity, which converts CPT-11 to its active form (7-ethyl-10-hydroxycamptothecin). Inhibition of the beta-glucuronidase activity in the intestinal microflora by antibiotics (1 mg penicillin and 2 mg streptomycin per ml of drinking water) markedly ameliorated the diarrhea and reduced cecal damage. Analysis of CPT-11 and its metabolites in the feces indicated that antibiotics completely inhibited the deconjugation of the glucuronic conjugate of 7-ethyl-10-hydroxycamptothecin by beta-glucuronidase. It is suggested that CPT-11-induced diarrhea would be attributable to the damage to the cecum, and that the inhibition of the beta-glucuronidase activity in the intestinal microflora is a major protective effect of antibiotics.

Animals↗
PubMed1977

[Beta-glucuronidase activity in human ovarian tissue during the life- and cycle-phases of the woman].

The behaviour of the beta-glucuronidase activity during the life phases and the phase of the cycle of a woman has been studied in 51 human ovaries after the Dohrmann method. The study clearly indicates a dependency on age, that is demonstrated by a rise in beta-glucuronidase activity from 536 microgram Ph/h/g ovarial tissue during full functioning to 705 microgram Ph/h/g ovarial tissue in the premenopause and by dropping to 529 microgram Ph/h/g ovarial tissue in the menopause and the senium. The premenopause values are significantly higher compared to that of the other two functional phases. The activity of the beta-glucuronidase is significantly higher in the secretory phase than in the proliferation phase. Existing relations between the beta-glucuronidase of the ovary and the gonadotropic hormones of the hypophysis and the oestrogen metabolism are discussed.

Adult↗