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)

The growth of L 1210 leukemia in DBA/2 strain mouse, provokes in the grafted animals intraleucocytic enzymatic modifications. As increase of acid phosphatase and a decrease of beta-glucuronidase were observed in the lymphocytes, the level of polymorphonuclear non-specific esterase being decreased. The implications of these modifications in the host response toward the tumor is discussed.
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PMID:[Cytochemical study of leucocytes of DBA/2 Mice after leukemia L1210 tumor graft]. 41 May 51

C57BL/K1, DBA/2/K1, and backcross male mice have been analyzed for H-2 type, serum testosterone level, and kidney beta-glucuronidase activity. No associations or correlations were found among these three parameters in the backcross material.
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PMID:Relationship among H-2 type, serum testosterone level, and kidney beta-glucuronidase activity in the mouse. 100 4

Kidney beta-glucuronidase activity in C57BL/K1 and DBA/2/K1 male mice differes about tenfold, C57 giving low and DBA high values. Another C57 subline, C57BL/6J, has slightly higher activity than C57BL/K1. There is an association between the kidney glucuronidase activity and coat color determined by the buff locus, which indicates that part of the variation is due to differences at the Gur locus. The bf allele per se raises the activity of the enzyme. The backcross distributions give evidence that at least one more locus is involved.
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PMID:Genetic effects on male mouse kidney glucuronidase activity. 100 8

Long-chain fatty acids inhibit glucuronidation of benzo(a)pyrene phenols in perfused liver; therefore, this study was designed to investigate interactions of fatty acids with beta-glucuronidase, glucuronosyl transferase, and energy supply. In beta-glucuronidase-deficient C3H/He mice, infusion of oleate (250 microM) increased the release of free benzo(a)pyrene phenols from 14 to 33 nmol/g/h and decreased release of glucuronides into the perfusate from 25 to 17 nmol/g/h. Rates of accumulation of glucuronides in the liver were also diminished from 11 to 4 nmol/g/h after infusion of oleate (250 microM). Fatty acids did not affect the release of benzo(a)pyrene metabolites into bile, and the ratio of free phenol to glucuronide production was increased from 0.57 to 1.30. A similar trend was observed in livers from DBA/2 mice that have beta-glucuronidase. Rates of hydrolysis of benzo(a)pyrene-O-glucuronide were not altered in isolated microsomes by addition of oleoyl coenzyme A (CoA) or octanoyl CoA (10- approximately 100 microM). Thus, we conclude that fatty acids do not alter glucuronidation by acting on beta-glucuronidase. The concentration of cofactors (UDP-glucuronic acid, UDP-glucose, and adenine nucleotides) involved in hepatic conjugation was not altered by infusion of concentrations of oleate (300 microM) that inhibited glucuronidation in perfused livers. When oleate concentrations were increased to 600 microM, UDP-glucuronic acid and UDP-glucose decreased 44 and 49%, respectively, and the ATP:ADP ratio declined concomitantly. Oleoyl CoA inhibited UDP-glucuronosyl transferase noncompetitively (half-maximal inhibition, 10 microM) in microsomes with 3-hydroxy-benzo(a)pyrene or p-nitrophenol as substrate. In contrast, octanoyl CoA was a very poor inhibitor of transferase activity. Inhibition of the transferase by oleoyl CoA was increased markedly by treatment with detergents (Triton X-100), i.e., half-inhibition of glucuronosyl transferase was obtained with about 2 microM oleoyl CoA. Inhibition of UDP-glucuronosyl transferase by oleoyl CoA was also increased in a dose-dependent manner by albumin, possibly due to increasing access of the CoA derivative to the enzyme. Collectively, these data indicate that fatty acids diminish glucuronidation via the formation of acyl CoA compounds that inhibit UDP-glucuronosyl transferase noncompetitively.
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PMID:Inhibition of glucuronidation of benzo(a)pyrene phenols by long-chain fatty acids. 190 48

Although the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), via its interaction with the Ah receptor, is an extremely potent carcinogen and immunosuppressive agent in experimental animals, its possible actions on polymorphonuclear (PMN) function have not been determined. In addition to their importance against infectious organisms, PMNs have been implicated in antitumor resistance. The present studies examined the effects of in vivo exposure to TCDD on PMN function in B6C3F1 (TCDD sensitive, presence of high affinity Ah receptor) and DBA/2N (TCDD resistant at low doses, defective Ah receptor) mice. Animals received a single oral exposure of 5 or 10 micrograms/kg of TCDD and PMNs were obtained 5 days later from the peritoneal cavity following elicitation with sodium caseinate. TCDD reduced the cytolytic and cytostatic activity of PMA-activated PMNs in B6C3F1, but not in DBA/2N mice, suggesting that this response segregates with the Ah locus. Furthermore, TCDD was found to bind specifically to PMNs from Ah-responsive mice. Neither the production of superoxide and hydrogen peroxide nor degranulation, the latter measured by beta-glucuronidase release, was impaired. Supernatants recovered from PMN cell cultures of TCDD-sensitive mice, but not from resistant DBA/2N mice, showed reduced killing capacity for actinomycin D-treated L929 tumor cells, while their ability to bind to tumor cells was not altered. These data suggest that TCDD interferes with PMN-mediated tumor cell killing by altering the production or secretion of a cytolytic factor. Examination of bone marrow stem cells revealed that granulocytic but not monocytic colonies were reduced after TCDD exposure in vivo and in vitro. Although mature PMNs had detectable levels of Ah receptor, exposure in vitro of these cells to TCDD had no effect on antitumor activity. Thus, it is possible that TCDD may affect PMNs at the level of hematopoiesis, via a direct interaction with granulocyte precursor cells, or modulate PMNs at different stages of maturation.
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PMID:Selective inhibition of polymorphonuclear neutrophil activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin. 255 88

Activities of 10 lysosomal hydrolase enzymes (beta-hexosaminidase, beta-galactosidase, alpha-galactosidase, alpha-mannosidase, beta-mannosidase, alpha-L-fucosidase, beta-glucuronidase, alpha-glucosidase, alpha-N-acetylgalactosaminidase, and acid phosphatase) were determined in eight organs (brain, liver, kidney, spleen, heart, skeletal muscle, lung, and testis) in males and females of six inbred mouse strains (C57BL/6J, C3H/HeJ, DBA/2J, BALB/cJ, P/J, and 129/J). Examples of enzyme-specific variation, organ-specific variation, and enzyme- and organ-specific variation were found. New enzyme-specific variants with the features of systemic regulators for alpha-L-fucosidase and beta-mannosidase were found. Known variants were detected. Organ-specific variants had some of the properties expected for a new class of genes affecting multiple enzymes: organ-specific regulators.
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PMID:Variation in ten lysosomal hydrolase enzyme activities in inbred mouse strains. 302 5

Niclosamide, a widely used anthelmintic drug in underdeveloped countries, is known to be mutagenic in the Salmonella typhimurium microsomal test system. The urine obtained from mice treated with niclosamide is mutagenic in the TA98 and TA1538 strains. Its effects on mouse-sperm morphology were evaluated in CD1 and (BALB/cJ x DBA/2J) F1 mice after 5 daily oral niclosamide doses of either 60, 80, 100 or 120 mg/kg. A statistically significant increase in abnormal sperm morphology was detected in both CD1 and (BALB/cJ x DBA/2J) F1 mice. No drug-related effects on testis weight nor on sperm count were observed in either genotype. Urine samples obtained from niclosamide-treated F1 mice were assayed with the Salmonella typhimurium strain TA1538 both in the absence and presence of beta-glucuronidase. In the absence of glucuronidase, urine mutagenicity increased with increasing dose and the highest doses were toxic. In the presence of glucuronidase, urine mutagenicity and toxicity also increased. Only at the highest dose (120 mg/kg), however, was there a positive correlation between the urine mutagenic activity and an increase in the number of abnormal sperm. The results of this study suggest that the increase in abnormal sperm depends on the systemic presence of non-conjugated niclosamide metabolites.
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PMID:Sperm shape abnormality and urine mutagenicity in mice treated with niclosamide. 327 17

Delayed toxicity of a single dose of 300 mg/kg cyclophosphamide (CP) was investigated in female DBA/2 mice. Lethality was low up to 30 days but increased markedly afterwards reaching a peak of 50% between 50-70 days with a total mortality of more than 80% by day 120 after CP. One week before death, the mice suffered a sharp loss of weight and showed typical signs of wasting disease. There was a decrease in the white cell count and lymphocyte neutrophil ratio was reversed as a result of lymphocyte depletion whereas neutrophil count remained similar to the controls. Profound lymphocyte depletion was also observed in light and electron microscopy preparations of thymus from mice with CP-induced wasting disease. Histochemical methods demonstrated increased activity of four lysosomal enzymes, acid phosphatase, beta-glucuronidase, E600 resistant esterase and n-acetyl-beta-glucosaminidase, in the thymus of treated mice. Acid phosphatase was notably active in thymus epithelial cells; the reaction product was localized in multiple primary Golgi lysosomes, Golgi cisternae, cisternae of the endoplasmic reticulum, and secondary lysosomes. The appearance of numerous cystic formations, as well as the activation of the lysosomal system and the presence of large areas of degradation support the assumption that CP-delayed toxicity is accompanied by thymus involution. Delayed mortality was partially prevented when syngenic bone marrow cells were injected as early as 24 h after CP injection. On the other hand thymus transplants were incapable of reducing delayed lethality. It is suggested that CP provokes a delayed wasting syndrome with thymic involution that is not caused by a direct effect on specific thymus structures but rather secondary to a primary injury to pre T cells in bone marrow.
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PMID:Delayed toxicity of cyclophosphamide in normal mice. 355 94

Serum beta-glucuronidase activity is shown to differ quantitatively in the following strains of mice, listed in order of increasing activity: C3H, C57BL/6 less than BALB/c, DBA/2, ICR less than SENCAR, A/He. The level of the enzyme in the murine strains is shown to correlate with the urinary excretion of 17-ketosteroids, which in turn reflects the endogenous level of androgens. Dietary calcium D-glucarate, an in vivo beta-glucuronidase inhibitor, reduced the steady state level of both beta-glucuronidase and 17-ketosteroid excretion in the highly susceptible A/He and SENCAR strains to that of strains known to be resistant to chemical carcinogenesis. Sensitivity of the A/He strain is significantly reduced by dietary calcium glucarate, which is shown to inhibit DNA binding and the induction of pulmonary adenomas by benzo[a]pyrene.
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PMID:Dietary glucarate-mediated reduction of sensitivity of murine strains to chemical carcinogenesis. 376 60

Two-cell embryos, obtained from the C57BL/6N and DBA/2N strains, were cultured in media that supported in vitro differentiation and that contained [3H]benzo[a]pyrene. High-pressure liquid chromatography of the activated intermediates formed during in vitro early embryonic development indicated that the onset of polynuclear aromatic hydrocarbon activation coincided with blastocyst formation. Comparison of individual oxygenated intermediates metabolically formed from embryos genetically "responsive" or "nonresponsive" to aromatic hydrocarbons revealed significant quantitative differences in the production of dihydrodiol, quinone, and phenolic derivatives. In addition to exhibiting basal mixed-function oxidase activity, blastocysts were also responsive to enzymatic induction when exposed to 2,-3,7,8-tetrachlorodibenzo-p-dioxin. The presence of operative metabolite-detoxifying pathways was also assayed. Enzymatic treatment of water-soluble metabolites with beta-glucuronidase or arylsulfatase revealed that neither glucuronic acid conjugates nor sulfate ester derivatives were present. These data, therefore, provide direct evidence that late preimplantation mouse embryos (day 3 1/2 of gestation) are similar to later developmental stages in having the enzymatic capability for xenobiotic activation and enzyme induction but are dissimilar with respect to their detoxification mechanism(s). Moreover, the ability of preimplantation embryos to activate directly polynuclear aromatic hydrocarbon to bioreactive intermediates may be of importance in assessing the ontological susceptibility of the developing embryo to carcinogenic or teratogenic chemicals.
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PMID:Developmental onset of mixed-function oxidase activity in preimplantation mouse embryos. 627 1


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