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)

Mouse kidney beta-glucuronidase production is under multihormonal control. In normal mice, kidney glucuronidase is induced over 100-fold by testosterone. However, hypophysectomy reduces this induction to about 5% of normal. This loss in inducibility was in part restored by growth hormone. Simultaneous administration to hypophysectomized female mice of growth hormone and testosterone, but not of prolactin and testosterone, restored kidney glucuronidase concentration to half that found in testosterone-treated normal female mice. Growth hormone alone had no effect in hypophysectomized females nor did it enhance glucuronidase activity in testosterone-treated normal females. Radiolabeling experiments demonstrated that the enhancement by growth hormone of glucuronidase activity was accompanied by a corresponding increase in its rate of synthesis. Kidney hypertrophy and kidney glucuronidase production may be under common hormonal regulation. Testosterone or growth hormone treatment alone of hypophysectomized mice had little or no effect on either process, but combined treatment with the two hormones significantly enhanced both. The rate of synthesis of kidney glucuronidase is controlled by the Gur gene. Relative differences in kidney glucuronidase synthesis in mice of different Gur genotype were maintained in testosterone-treated hypophysectomized mice. This suggests that control of glucuronidase synthesis by the Gur locus is exerted by interaction with androgens rather than pituitary products.
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PMID:Roles of growth hormone and testosterone in the synthesis of mouse kidney glucuronidase. 72 3

Androsterone, etiocholanolone, pregnanetriol, dehydroepiandrosterone, pregnanediol, tetrahydrocortisol, 5-pregnenolone and 11-beta-OH-androsterone were incubated with beta-glucuronidase preparations (Helix pomatia, bovine liver and E. coli) for 96 hrs at 37 degrees C. After extraction and silylation they were gas-chromatographed. The first 3 steroids were left practically intact. The least decomposition of the last 5 steroids occurred with the liver enzyme. Testosterone and 11-ketoandrosterone without the enzymes showed 74 and 35% recoveries. Cortisol and tetrahydrocortisol, incubated with the first two enzymes for 18 hrs at 37 degrees and 48 degrees C, showed nearly 100% recoveries. The recoveries of 17-OHCS in urines (pH 7.8-8.8), stored for 7 days, was 80% at 20 degrees-25 degrees C and 55% at 25 degrees-30 degrees C. The same samples, brought to pH 1.8-2.8 WITH NaHSO4 before the storage, showed a 100% recovery.
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PMID:[Decomposition of steroids during incubation with beta-glucuronidase and during storage of urine]. 76 25

A method was developed for measuring in vivo rates of mRNA synthesis in mice by pulse-labeling with the RNA precursor [3H]orotate and then using hybridization to recover specific mRNAs. The efficiency of recovery is determined with synthetic RNAs as internal hybridization standards. The method is particularly applicable to the kidney since this organ shows a strong preferential uptake of the label. Rates of synthesis, expressed as a fraction of total RNA synthesis, were measured for the androgen-inducible mRNAs coding for beta-glucuronidase (GUS), ornithine decarboxylase (ODC), the protein coded by the RP-2 gene, and the so-called kidney androgen-regulated protein (KAP). Control mRNAs coded for beta-actin, phosphoenolpyruvate carboxykinase, and major urinary protein. Testosterone markedly increased the synthesis of the androgen-inducible mRNAs, but not the control mRNAs. Induction was not seen in mutant mice lacking functional androgen receptor protein. For GUS, ODC, and RP-2 mRNAs, the fold induction of synthesis was less than the fold induction of concentration, suggesting that mRNA stabilization also plays a part in the response to androgen. For GUS, ODC, and RP-2 mRNAs, but not KAP mRNA, induction of synthesis was rapidly reversed after testosterone removal. KAP mRNA was also exceptional in that its concentration was disproportionately high compared with its rate of synthesis, implying that it is a particularly stable mRNA.
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PMID:mRNA synthesis rates in vivo for androgen-inducible sequences in mouse kidney. 338 33

The data only, in the form of mean, variance, and range, by age and sex, are tabulated for excretion of 17-ketosteroids, pregnanes, and testosterone in 24-hour urines of 419 males and 269 females. The metabolites were androsterone, etiocholanolone, dehydroepiandrosterone, 11-keto-androsterone, 11-keto-etiocholanolone, 11beta-hydroxy-androsterone, 11beta-hydroxy-etiocholanolone, pregnanediol, and pregnanetriol. Persons under 20 years were clinic patients or residents of institutions; all had bone age determined. Persons over 20 were hospital personnel or patients. Methods of analysis included hydrolysis with beta-glucuronidase and arylsulfatase, acid hydrolysis, ether extraction, and gas chromatography. Testosterone metabolites were chromatographed on columns and thin layers before gas chromatography.
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PMID:[The excretion of 17-oxosteroids, pregnanes and testosterone in human urine and the dependency on age and sex (author's transl)]. 480 55

1. [4-(14)C]Testosterone was administered to anaesthetized male and female New Zealand White rabbits as a single injection or as a 45-60min. infusion. 2. After a single dose a total of approx. 56-80% of the radioactivity was excreted in bile and urine. After infusion total recovery of radioactivity was approx. 63-75%. 3. The mean ratio of metabolites in urine to those in bile was 0.77+/-0.41 (range 0.3-1.5). 4. Bile and urine samples were hydrolysed successively by beta-glucuronidase, cold acid and hot acid. In both bile and urine neutral metabolites extracted by ethyl acetate-ether were found mainly after beta-glucuronidase hydrolysis, but a considerable proportion of the dose was converted into substances not extractable from alkaline aqueous solution after all forms of hydrolysis used.
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PMID:Steroid metabolism in the rabbit. Biliary and urinary excretion of metabolites of [4-14-C]testosterone. 603 16

The ventricular myocardium was studied in A/J mice and in Sprague-Dawley rats. In male mice, the ventricles were slightly larger and the specific activities of the lysosomal hydrolases, beta-glucuronidase, hexosaminidase, beta-galactosidase, and arylsulphatase, and the inner mitochondrial enzyme cytochrome c oxidase were substantially higher than in female mice. Orchiectomy abolished this sex difference. Testosterone administration induced myocardial hypertrophy and accretion of RNA and protein without altering the DNA, and substantial increases in the activities of the lysosomal hydrolases and cytochrome c oxidase. However, the mitochondrial membrane enzyme monoamine oxidase was unaffected by sex, orchiectomy, and testosterone administration. Heart lysosomes from male mice showed a smaller structure-linked latency of the lysosomal enzymes and a greater fragility of the lysosomal membrane to osmotic and mechanical stress than those from female mice. This sex difference was also abolished by orchiectomy and restored by testosterone replacement. Similar sex differences were observed in the rat with respect to heart size, acid hydrolase activities, and lysosomal enzyme latency and membrane stability. These findings indicate that endogenous androgens regulate myocardial cell growth, the activity of enzymes associated with lysosomes and the inner mitochondrial membrane, and some physiochemical properties of lysosomes.
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PMID:Testosterone-mediated sexual dimorphism of the rodent heart. Ventricular lysosomes, mitochondria, and cell growth are modulated by androgens. 704 2

Testosterone administration to female mice for 25 days produced a 70% increase in total kidney protein in both A/J and C57BL/6J mice. This is in contrast to the known androgen-responsive proteins, such as beta-glucuronidase and alcohol dehydrogenase, which each represent less than 1% of the total kidney proteins even after maximum stimulation. To investigate this discrepancy, we initiated a study to identify major proteins which increase with androgen treatment. Three new cytoplasmic proteins designated T1, T2, and T3 were found in different subcellular fractions of both A/J and C57BL/6J mice. T1 (43,000 daltons) and T2 (60,000 daltons) were found in the mitochondrial-lysosomal fraction of 25-day androgen-treated mice. T3 (54,000 daltons) was found in the microsomal fraction. Each of these proteins increased several-fold during androgen treatment, so that they were easily identified using sodium dodecyl sulfate polyacrylamide gel electrophoresis. By contrast, no major changes were noted in the soluble proteins. A nonhistone chromosomal protein of 54,000 mol wt (T4) was found in chromatin preparations from androgen-stimulated A/J mice. Additional studies with androgen-insensitive Tfm/Y mice and with various hormones indicated that stimulation of the T proteins was dependent on androgenic steroid and a functional androgen receptor.
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PMID:New androgen-stimulated proteins in the kidneys of female mice. 735 32

We have determined the effects of the Niemann-Pick type C (NPC) lesion, which impairs transport of cholesterol from lysosomes, on the androgenic status of male NPC mice. The mice have low serum testosterone levels resulting from decreased testosterone secretion. Testosterone secretion is reduced in NPC mouse testes incubated with 8-bromo-cAMP, 20 alpha-hydroxycholesterol, and pregnenolone compared to testosterone release by normal mouse testes under identical conditions. Ultrastructural examination of testes revealed a paucity of lipid droplets, extensive accumulation of inclusion bodies, and distorted endoplasmic reticulum in Leydig cells of adult NPC mice. The hypoandrogenemia caused systemic deficiencies in NPC mice. Seminal vesicles, a testosterone-responsive tissue, were underdeveloped in NPC male mice. The testosterone-responsive kidney beta-glucuronidase activity was also underexpressed. Seminal vesicle mass and beta-glucuronidase activity were increased by testosterone treatment of NPC mice. Many hepatic proteins, identified by microsequencing, were also deficient in NPC male mice. Levels of alpha 2-mu-globulin, glutathione S-transferase-pi, carbonic anhydrase-III, and selenium-binding protein increased in normal male mice during puberty, but did not increase in the NPC male mice. Based on the increases in protein expression during puberty, differential expression in males and females, and the reported involvement of androgens in regulating expression of some of these proteins, deficient expression of most of these proteins in male NPC mice appears to result from low testosterone levels. We conclude that a defect in testicular testosterone production in NPC male mice causes a pleiotropic deficiency in androgen-sensitive expression of proteins in various organs.
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PMID:The murine Niemann-Pick type C lesion affects testosterone production. 824 19

The expression and androgen regulation of beta-glucuronidase molecular forms were examined in mouse epididymis, liver, and kidney. Two-dimensional polyacrylamide gel electrophoresis performed under nondenaturing conditions showed that, compared to liver and kidney, which contain four microsomal (M1-M4) and a major lysosomal (L) form of beta-glucuronidase, the epididymis revealed regional differences and tissue specificity in the expression of the various molecular forms of the enzyme. Only the lysosomal form (pI 5.4-6.1) is present in the caput epididymidis while the corpus/cauda contains the lysosomal form, the free X form (pI 5.9-6.3) and the four microsomal forms (X form complexed with egasyn). Mutant mice that lack egasyn have no microsomal forms in the distal epididymis. In epididymal fluid, the lysosomal form is found throughout the epididymis, whereas the X form appears only in the corpus/cauda epididymidis. Sodium dodecyl Sulfate (SDS)-gel electrophoresis and western blot analysis of immunoprecipitated beta-glucuronidase revealed only one band corresponding to the L form (apparent molecular weight 74 kDa) in the caput epididymidis and two bands in the corpus/cauda (apparent molecular weights 73 and 75 kDa), corresponding to L and X forms, respectively. Castration of mice led to the suppression of the regional differences in the appearance of X and M forms in the epididymis. Testosterone supplementation to castrated mice restored the characteristic electrophoretic pattern of beta-glucuronidase in the caput epididymidis. In the liver and kidney, castration has no effect on the expression of the molecular forms, whereas androgen treatment induced the X form in the kidney. Histochemical localization of beta-glucuronidase confirmed the region specificity seen in the epididymis and in addition revealed cell specificity in the expression of beta-glucuronidase. These results indicate that beta-glucuronidase shows tissue specificity and, in the case of the epididymis, region and cell specificity. In addition, the enzyme in the different tissues responds differentially to androgens.
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PMID:Androgen regulation of molecular forms of beta-D-glucuronidase in the mouse epididymis: comparison with liver and kidney. 879 10

The human epididymis and its secretions actively promote sperm fertilizing capacity and provide protection for spermatozoa against harmful influences. Among epididymal secretions, glycosidases have been recently studied and associated with molecular changes on the sperm surface. In the present work, we studied the influence of different concentrations of testosterone, dihydrotestosterone and cyproterone acetate on the secretion of alpha-glucosidase, N-acetyl-glucosaminidase, beta-glucuronidase and alpha-mannosidase by isolated and cultured epithelial cells from human caput, corpus and cauda epididymides. Cell cultures were obtained from aggregates of isolated tubule fragments plated on extracellular matrix-covered multi-well plates. Activities of the glycosidases were measured in conditioned culture media and were higher in the distal regions of the epididymis. Testosterone and dihydrotestosterone significantly increase the enzyme secretion in a concentration-dependent manner. This increase was higher in corpus and/or cauda than in caput epididymis. Cyproterone acetate caused a dose-dependent decrease in glycosidase secretion in cultures from all epididymal regions. It is concluded that the secretion of epididymal glycosidases is regulated by androgen, being stimulated by dihydrotestosterone and testosterone and inhibited by the androgen antagonist cyproterone acetate.
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PMID:Androgen regulation of glycosidase secretion in epithelial cell cultures from human epididymis. 1035 69


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