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)

We evaluated the biochemical characteristics of endogenous fluorescent substances, Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm, present in sera of patients with chronic renal failure (Clin. Chem. 31:1988, 1985). Sera from 23 patients with chronic renal failure (CRF) and from 10 normal subjects were filtered through ultrafiltration membranes (cutoff limit of 500 Da). Fluorescence intensity of the aforementioned substances was significantly elevated as compared to normals (p less than 0.001). Fluorescence characteristics of these substances remained unaltered after ultrafiltration and treatment with beta-glucuronidase. Extraction of these fluorescent compounds with organic solvents (dichloromethane, ethyl acetate, chloroform:methanol) could not be achieved after ultrafiltrates were subjected to 6N hydrochloric acid (HC1) hydrolysis. In addition, treatment with 6N HC1 enhanced fluorescence intensity without altering fluorescence excitation/emission maxima. Removal of fluorescence could be accomplished in toto by adsorption onto activated charcoal with subsequent recovery from charcoal by treatment with sodium hydroxide, pH 12 (Ex 380 nm: 51.1%, Ex 400 nm: 91.8%). Analysis of alkali-treated specimens by high performance liquid chromatography demonstrated that peptides associated with these fluorescent substances were denatured, although fluorescence at these previously described excitation/emission maxima persisted. Our studies indicate that the unique fluorescence observed in the sera of patients with CRF is not an intrinsic characteristic of a specific peptide or its amino acids, but rather an inherent property of fluorescent molecules which may bind to these peptides.
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PMID:Biochemical elucidation and HPLC fractionation of fluorescent peptides in patients with chronic renal failure. 344 37

A method has been developed for the simultaneous determination of antipyrine and its three major metabolites in plasma of patients with renal failure. Plasma samples (500 microl) were hydrolyzed with beta-glucuronidase/aryl sulphatase. The compounds, after addition of sodium chloride, were extracted with chloroform:ethanol (90:10, v/v) in acidic medium. Chromatographic conditions comprise a C18 column, a mobile phase with 30% methanol and 70% 0.25N sodium acetate buffer (pH 5.0), a total run time of 10 minutes, and ultraviolet absorbance detection at 254 nm. Confidence limits showed 0.5 to 40.0 microg/ml(-1) linearity (r2 = 0.999); 0.1 microg/ml(-1) HMA, 0.05 microg/ml(-1) antipyrine and NORA, and 0.5 microg/ml(-1) OHA sensitivity and absolute recovery >95%. Interprecision and intraprecision expressed as coefficient of variation were <10% for all compounds investigated. The assay shows to be suitable for pharmacokinetics and drug metabolism studies after administration of a single oral dose of 500 mg of antipyrine to a patient with hypertension and chronic renal failure (CL(CR) = 34.17 ml/min(-1); 1.73 m(-2)).
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PMID:Determination of antipyrine and metabolites in plasma of a patient with mild renal failure. 942 Nov 15

Changes in the expression of klotho, a beta-glucuronidase, contribute to the development of features that resemble those of premature aging, as well as chronic renal failure. Klotho knockout mice have increased expression of the sodium/phosphate cotransporter (NaPi2a) and 1alpha-hydroxylase in their kidneys, along with increased serum levels of phosphate and 1,25-dihydroxyvitamin D. These changes are associated with widespread soft-tissue calcifications, generalized tissue atrophy, and a shorter lifespan in the knockout mice. To determine the role of the increased vitamin D activities in klotho knockout animals, we generated klotho and 1alpha-hydroxylase double-knockout mice. These double mutants regained body weight and developed hypophosphatemia with a complete elimination of the soft-tissue and vascular calcifications that were routinely found in klotho knockout mice. The markedly increased serum fibroblast growth factor 23 and the abnormally low serum parathyroid hormone levels, typical of klotho knockout mice, were significantly reversed in the double-knockout animals. These in vivo studies suggest that vitamin D has a pathologic role in regulating abnormal mineral ion metabolism and soft-tissue anomalies of klotho-deficient mice.
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PMID:Reversal of mineral ion homeostasis and soft-tissue calcification of klotho knockout mice by deletion of vitamin D 1alpha-hydroxylase. 1944 69