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 intestinal first pass metabolism of amygdalin has been investigated in rat small intestine in vitro. The results show that amygdalin is hydrolyzed to prunasin, essentially in the wall of the proximal jejunum. This specific beta(1-6)hydrolytic cleavage of the terminal glucose residue is pH-dependent and can be inhibited by glucono-delta-lactone, a potent inhibitor of the lysosomal beta-glucosidase of the rat intestine. No substrate competition between phloridzin and lactose vs amygdalin was noted. None of the more common soluble beta- or alpha-enzymatic activities of mammalian intestine (alpha-glucosidase, alpha-amylase) or mammalian liver (beta-galactosidase, beta-glucuronidase) were capable of catalyzing the hydrolysis of the terminal glucose from amygdalin at pH's 5.0, 7.0 or 9.0. Furthermore, no metabolic activity of isolated rat livers toward amygdalin and prunasin was observed within two hours of recirculating perfusion. However, cecal contents of conventional rats, exhibited both amygdalin- and prunasin-hydrolyzing activities. The resulting mandelonitrile dissociates spontaneously into cyanide and benzaldehyde. Therefore, our findings indicate that metabolism of amygdalin to prunasin occurring in the proximal part of jejunum is apparently mediated by enzymatic beta(1-6)glucosidase activity of the gut wall. In contrast, the toxicity of amygdalin due to the release of cyanide obviously requires microbiological activities of the gut flora.
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PMID:Intestinal first pass metabolism of amygdalin in the rat in vitro. 308 25

A number of 2-(furan-2-yl)-4-phenoxyquinoline derivatives have been synthesized and evaluated for anti-inflammatory evaluation. 4-[(2-Furan-2-yl)quinolin-4-yloxy]benzaldehyde (8), with an IC(50) value of 5.0 microM against beta-glucuronidase release, was more potent than its tricyclic furo[2,3-b]quinoline isomer 3a (>30 microM), its 4'-COMe counterpart 7 (7.5 microM), and its oxime derivative 13a (11.4 microM) and methyloxime derivative 13b (>30 microM). For the inhibition of lysozyme release, however, oxime derivative 12a (8.9 microM) and methyloxime derivative 12b (10.4 microM) are more potent than their ketone precursor 7 and their respective tricyclic furo[2,3-b]quinoline counterparts 4a and 4b. Among them, 4-[4-[(2-furan-2-yl)-quinolin-4-yloxy]phenyl]but-3-en-2-one (10) is the most active against lysozyme release with an IC(50) value of 4.6 microM, while 8 is the most active against beta-glucuronidase release with an IC(50) value of 5.0 microM. (E)-1-[3-[(2-Furan-2-yl)quinolin-4-yloxy]phenyl] ethanone oxime (11a) is capable of inhibiting both lysozyme and beta-glucuronidase release with IC(50) values of 7.1 and 9.5 microM, respectively. For the inhibition of TNF-alpha formation, 1-[3-[(2-furan-2-yl)quinolin-4-yloxy]phenyl]ethanone (6) is the most potent with an IC(50) value of 2.3 microM which is more potent than genistein (9.1 microM). For the inhibitory activity of fMLP-induced superoxide anion generation, 11a (2.7 microM), 11b (2.8 microM), and 13b (2.2 microM) are three of the most active. None of above compounds exhibited significant cytotoxicity.
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PMID:Synthesis, cytotoxicity, and anti-inflammatory evaluation of 2-(furan-2-yl)-4-(phenoxy)quinoline derivatives. Part 4. 1652 34