Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inhibitory potency of the antiallergic compounds picumast (PIC; Boehringer Mannheim) and ketotifen (K; Sandoz) on the release of 3 preformed and 3 newly generated inflammatory mediators was estimated as an indicator for their antiallergic activity. Peripheral human leukocytes (HL) or rat alveolar macrophages (RAM) were stimulated by opsonized zymosan (C3-Z) and/or anti-IgE antibody, following preincubation times with PIC and K. SRS-A was measured with the help of a guinea pig ileum bioassay, PGE2 and TxB2 by RIA (NEN), histamine (H) by an automated fluorimetric procedure, tryptic proteinase (P) by a colorimetric test employing Tos-Gly-Pro-Arg-pNA (Chromozym TH; Boehringer Mannheim) as chromogenic substrate and beta-glucuronidase (beta-G) by a colorimetric test (Sigma). PIC (IC30: 2 X 10(-5) mol/l) was 100 times more potent than K as inhibitor of the anti-IgE-induced release of H and P and also 5 times more potent as inhibitor of SRS-A-formation/release in/from HL. In contrast, on RAM, K (IC30: 7 X 10(-6) mol/l) had a 3 times greater potency as inhibitor of the C3-Z-induced SRS-A formation and suppressed PGE2 release (4 X 10(-5)-2 X 10(-4) mol/l), whereas PIC (2 X 10(-5) mol/l) potentiated PGE2 release remarkably. TxB2 release from RAM was inhibited nearly equipotently by PIC and K. beta-G release was strongly potentiated by K (greater than or equal to 8 X 10(-6) mol/l), but weakly inhibited by PIC (2 X 10(-5) mol/l). PIC (greater than or equal to 4 X 10(-5) mol/l) also increased the beta-G release and in the same manner the anti-IgE- or C3-Z-induced release of other 'preformed' mediators like H and P from HL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition profiles of picumast and ketotifen on the in vitro release of prostanoids, slow-reacting substance of anaphylaxis, histamine and enzyme from human leukocytes and rat alveolar macrophages. 243 54

Procedures based on high-performance liquid chromatography (HPLC) were developed for identifying and measuring p-aminobenzoic acid (PABA) and its conjugate metabolites in human urine after oral doses of PABA. p-Aminohippuric acid (PAH), PABA, p-acetamidohippuric acid (PAHA) and p-acetamidobenzoic acid (PADB) in urine were resolved and determined by HPLC simultaneously and directly without extraction. A mobile phase consisting of 3% (v/v) acetonitrile in distilled water containing 0.005 M 1-heptanesulphonic acid in glacial acetic acid (PIC-B7) at pH 3.3 was eluted at 1 ml/min through a C18 Spherisorb column, followed by UV detection at 280 nm. After hydrolysis of urine samples at 37 degrees C for 3 h with beta-glucuronidase, the amounts of PABA-glucuronide and PADB-glucuronide were also determined. The retention times of PAH, a dominant peak which disappeared after hydrolysis, PABA, DABA (3,5-diaminobenzoic acid, as the internal standard), PAHA and PADB were 11.8, 14, 15, 18, 24 and 46 min, respectively. The 24-h urinary recoveries of PAH, PAHA, PADB, PADB-glucuronide, PABA and PABA-glucuronide after separate oral doses of 200 and 800 mg of PABA in one healthy subject were 43.4 and 48.1, 7 and 29.1, 11.2 and 11.8, 34.8 and 6.6, 0.2 and 0.3, and 1.0 and 2.4%, respectively. It is interesting that at high dose (800 mg) saturation of glucuronidation of PADB (N-acetylated PABA) appeared to occur, which resulted in an increase in the formation of PAHA, the glycine conjugate of PADB. Over 90% of the oral dose was accounted for by 8 h after administration.
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PMID:Direct and simultaneous high-performance liquid chromatographic assay for the determination of p-aminobenzoic acid and its conjugates in human urine. 326 Feb 39