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dc.contributor.authorBerge, G
dc.contributor.authorOvrebo, S
dc.contributor.authorBotnen, IV
dc.contributor.authorHewer, A
dc.contributor.authorPhillips, DH
dc.contributor.authorHaugen, A
dc.contributor.authorMollerup, S
dc.date.accessioned2018-09-11T10:19:46Z
dc.date.issued2004-07-19
dc.identifier2
dc.identifier.citationBRITISH JOURNAL OF CANCER, 2004, 91 pp. 333 - 338
dc.identifier.issn0007-0920
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2623
dc.identifier.doi10.1038/sj.bjc.6601898
dc.description.abstractResveratrol ( trans-3,4’,5-trihydroxystilbene), a phytoalexin present in various plants and foods, has in several in vitro and in vivo studies demonstrated cancer chemopreventive and chemotherapeutic potential. We investigated the in vitro effect of resveratrol on benzo[ a] pyrene ( B[ a] P)-induced DNA adducts in human bronchial epithelial cells. This was compared to the effect of resveratrol on the expression of the cytochrome P450 (CYP) genes CYP1A1 and CYP1B1 and the formation of B[ a] P metabolites. Exposure of BEAS-2B and BEP2D cells to B[ a] P and increasing concentrations of resveratrol resulted in a dose- and time-dependent inhibition of DNA adduct formation quantified by P-32-postlabelling. Supporting this result, resveratrol was shown to inhibit CYP1A1 and CYP1B1 gene expression, as measured by real-time reverse transcriptase - polymerase chain reaction. Also, a significant correlation was found between the number of DNA adducts and the mRNA levels of these genes. Using HPLC analysis, a concomitant decrease in the formation of B[ a]P-derived metabolic products was detected. In conclusion, these data lend support to a chemopreventive role of resveratrol in polycyclic aromatic hydrocarbon-induced carcinogenesis.
dc.format.extent333 - 338
dc.languageeng
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleResveratrol inhibits benzo[a]pyrene-DNA adduct formation in human bronchial epithelial cells
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/sj.bjc.6601898
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2004-07-19
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfBRITISH JOURNAL OF CANCER
pubs.notesaffiliation: Mollerup, S (Reprint Author), Norwegian Inst Occupat Hlth, Dept Toxicol, POB 8149 Dep, N-0033 Oslo, Norway. Norwegian Inst Occupat Hlth, Dept Toxicol, N-0033 Oslo, Norway. Inst Canc Res, Sect Mol Carcinogenesis, Sutton SM2 5NG, Surrey, England. keywords: DNA adducts; cytochrome P450; human bronchial epithelial cells; metabolites; PAH; real-time RT-PCR; resveratrol keywords-plus: ARYL-HYDROCARBON RECEPTOR; LUNG-CANCER; CYP1A1 EXPRESSION; CIGARETTE-SMOKING; ALCOHOL INTAKE; TUMOR-GROWTH; DNA-DAMAGE; APOPTOSIS; CARCINOMA; WINE research-areas: Oncology web-of-science-categories: Oncology author-email: [email protected] orcid-numbers: Phillips, David/0000-0001-8509-3485 number-of-cited-references: 36 times-cited: 26 usage-count-last-180-days: 0 usage-count-since-2013: 1 journal-iso: Br. J. Cancer doc-delivery-number: 841LC unique-id: ISI:000222930300024 oa: gold_or_bronze da: 2018-09-10
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Human Biomonitoring & Carcinogen Activation
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Human Biomonitoring & Carcinogen Activation
pubs.volume91en_US
pubs.embargo.termsNot known
icr.researchteamHuman Biomonitoring & Carcinogen Activationen_US
dc.contributor.icrauthorPhillips, David Hunteren
dc.contributor.icrauthorHewer, Alanen


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