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Article: Trapping of phenylacetaldehyde as a key mechanism responsible for naringenin's inhibitory activity in mutagenic 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine formation

TitleTrapping of phenylacetaldehyde as a key mechanism responsible for naringenin's inhibitory activity in mutagenic 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine formation
Authors
Issue Date2008
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/crt
Citation
Chemical Research In Toxicology, 2008, v. 21 n. 10, p. 2026-2034 How to Cite?
AbstractChemical model reactions were carried out to investigate the mechanism of inhibition by a citrus flavonoid, naringenin, on the formation of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP), the most abundant mutagenic heterocyclic amine found in foods. GC-MS showed that naringenin dose dependently reduced the level of phenylacetaldehyde, a key intermediate on the pathway to the formation of PhIP. Subsequent LC-MS analyses of samples from a wide range of model systems consisting of PhIP precursors, including phenylalanine, glucose, and creatinine, suggested that naringenin scavenged phenylacetaldehyde via adduct formation. An isotope-labeling study showed that the postulated adducts contain fragment(s) of phenylalanine origin. Direct reaction employing phenylacetaldehyde and naringenin further confirmed the capability of naringenin to form adducts with phenylacetaldehyde, thus reducing its availability for PhIP formation. Two of the adducts were subsequently isolated and purified. Their structure was elucidated by one- and two-dimensional NMR spectroscopy as 8-C-(E-phenylethenyl)nar-ingenin (1) and 6-C-(E-phenylethenyl)naringenin (2), respectively, suggesting that C-6 and C-8 are two of the active sites of naringenin in adduct formation. These two adducts were also identified from thermally processed beef models, highlighting phenylacetaldehyde trapping as a key mechanism of naringenin to inhibit PhIP formation. © 2008 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/157532
ISSN
2015 Impact Factor: 3.025
2015 SCImago Journal Rankings: 1.323
ISI Accession Number ID
Funding AgencyGrant Number
HKSAR Research Grand CouncilHKU 7778/07M
Funding Information:

We thank the HKSAR Research Grand Council for financial support (Project HKU 7778/07M to M.W.).

References

 

DC FieldValueLanguage
dc.contributor.authorCheng, KWen_HK
dc.contributor.authorWong, CCen_HK
dc.contributor.authorCho, CKen_HK
dc.contributor.authorChu, IKen_HK
dc.contributor.authorSze, KHen_HK
dc.contributor.authorLo, Cen_HK
dc.contributor.authorChen, Fen_HK
dc.contributor.authorWang, Men_HK
dc.date.accessioned2012-08-08T08:51:01Z-
dc.date.available2012-08-08T08:51:01Z-
dc.date.issued2008en_HK
dc.identifier.citationChemical Research In Toxicology, 2008, v. 21 n. 10, p. 2026-2034en_HK
dc.identifier.issn0893-228Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/157532-
dc.description.abstractChemical model reactions were carried out to investigate the mechanism of inhibition by a citrus flavonoid, naringenin, on the formation of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP), the most abundant mutagenic heterocyclic amine found in foods. GC-MS showed that naringenin dose dependently reduced the level of phenylacetaldehyde, a key intermediate on the pathway to the formation of PhIP. Subsequent LC-MS analyses of samples from a wide range of model systems consisting of PhIP precursors, including phenylalanine, glucose, and creatinine, suggested that naringenin scavenged phenylacetaldehyde via adduct formation. An isotope-labeling study showed that the postulated adducts contain fragment(s) of phenylalanine origin. Direct reaction employing phenylacetaldehyde and naringenin further confirmed the capability of naringenin to form adducts with phenylacetaldehyde, thus reducing its availability for PhIP formation. Two of the adducts were subsequently isolated and purified. Their structure was elucidated by one- and two-dimensional NMR spectroscopy as 8-C-(E-phenylethenyl)nar-ingenin (1) and 6-C-(E-phenylethenyl)naringenin (2), respectively, suggesting that C-6 and C-8 are two of the active sites of naringenin in adduct formation. These two adducts were also identified from thermally processed beef models, highlighting phenylacetaldehyde trapping as a key mechanism of naringenin to inhibit PhIP formation. © 2008 American Chemical Society.en_HK
dc.languageengen_US
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/crten_HK
dc.relation.ispartofChemical Research in Toxicologyen_HK
dc.subject.meshAcetaldehyde - Analogs & Derivatives - Chemistryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCattleen_US
dc.subject.meshFlavanones - Pharmacologyen_US
dc.subject.meshImidazoles - Chemistry - Metabolismen_US
dc.subject.meshMass Spectrometryen_US
dc.subject.meshMeaten_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMolecular Structureen_US
dc.subject.meshMutagenesis - Drug Effectsen_US
dc.titleTrapping of phenylacetaldehyde as a key mechanism responsible for naringenin's inhibitory activity in mutagenic 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine formationen_HK
dc.typeArticleen_HK
dc.identifier.emailChu, IK: ivankchu@hku.hken_HK
dc.identifier.emailSze, KH: khsze@hku.hken_HK
dc.identifier.emailLo, C: clivelo@hkucc.hku.hken_HK
dc.identifier.emailChen, F: sfchen@hku.hken_HK
dc.identifier.emailWang, M: mfwang@hku.hken_HK
dc.identifier.authorityChu, IK=rp00683en_HK
dc.identifier.authoritySze, KH=rp00785en_HK
dc.identifier.authorityLo, C=rp00751en_HK
dc.identifier.authorityChen, F=rp00672en_HK
dc.identifier.authorityWang, M=rp00800en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1021/tx800220hen_HK
dc.identifier.pmid18702534-
dc.identifier.scopuseid_2-s2.0-55949097344en_HK
dc.identifier.hkuros155635-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-55949097344&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issue10en_HK
dc.identifier.spage2026en_HK
dc.identifier.epage2034en_HK
dc.identifier.isiWOS:000260148300019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheng, KW=12141247000en_HK
dc.identifier.scopusauthoridWong, CC=35333095100en_HK
dc.identifier.scopusauthoridCho, CK=25642646600en_HK
dc.identifier.scopusauthoridChu, IK=7103327484en_HK
dc.identifier.scopusauthoridSze, KH=7006735061en_HK
dc.identifier.scopusauthoridLo, C=15737175700en_HK
dc.identifier.scopusauthoridChen, F=7404907980en_HK
dc.identifier.scopusauthoridWang, M=7406691844en_HK

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