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Quercetin acts as an antioxidant and downregulates CYP1A1 and CYP1B1 against DMBA-induced oxidative stress in mice

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dc.contributor.authorChoi, Eun Jeong-
dc.contributor.authorKim, Taehee-
dc.contributor.authorKim, Gun-Hee-
dc.date.available2021-02-22T12:46:10Z-
dc.date.issued2012-07-
dc.identifier.issn1021-335X-
dc.identifier.issn1791-2431-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11878-
dc.description.abstractWe investigated the effects of quercetin on 7,12-dimethylbenz(a)anthracene (DMBA)-induced oxidative stress and the expression of CYP1A1 and CYP1B1 in mice. Quercetin was administered orally to mice at 100 or 250 mg/kg BW for 18 days, after which DMBA (34 mg/kg BW) was administered intragastrically twice. Quercetin showed side effects such as increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in DMBA-untreated mice. Also, quercetin induced AST and ALT in DMBA-treated, although this was not significantly different from levels in DMBA-treated controls. The thiobarbituric acid reactive substances (TBARS) value showed a tendency to decrease following quercetin treatment; these decreases were significantly greater in the DMBA-treated compared to the untreated groups. Also, catalase and superoxide dismutase (SOD) activities as well as their mRNA expression were increased by quercetin; this increase was more pronounced in DMBA-treated compared to untreated mice. DMBA induced CYP1 activity as well as expression of CYP1A1 and CYP1B1. Each of these effects was significantly reduced by quercetin; however, this reduction was observed for CYP1A1 at only the higher dose and for CYP1B1 at both doses. These data suggest that quercetin shows antioxidant activity against DMBA-induced oxidative stress. Moreover, its regulation of CYP1A1 and CYP1B1 suggests the potential of quercetin as an anticancer supplement.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherSPANDIDOS PUBL LTD-
dc.titleQuercetin acts as an antioxidant and downregulates CYP1A1 and CYP1B1 against DMBA-induced oxidative stress in mice-
dc.typeArticle-
dc.publisher.location그리이스-
dc.identifier.doi10.3892/or.2012.1753-
dc.identifier.scopusid2-s2.0-84861536632-
dc.identifier.wosid000304638900041-
dc.identifier.bibliographicCitationONCOLOGY REPORTS, v.28, no.1, pp 291 - 296-
dc.citation.titleONCOLOGY REPORTS-
dc.citation.volume28-
dc.citation.number1-
dc.citation.startPage291-
dc.citation.endPage296-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusBUCCAL POUCH CARCINOGENESIS-
dc.subject.keywordPlusLOW-DENSITY-LIPOPROTEIN-
dc.subject.keywordPlusBLACK TEA POLYPHENOLS-
dc.subject.keywordPlusDNA ADDUCT FORMATION-
dc.subject.keywordPlusBREAST-CANCER-
dc.subject.keywordPlusMETABOLIC-ACTIVATION-
dc.subject.keywordPlusDIETARY FLAVONOIDS-
dc.subject.keywordPlusHEPG2 CELLS-
dc.subject.keywordPlusA549 CELLS-
dc.subject.keywordPlusRATS-
dc.subject.keywordAuthorantioxidant-
dc.subject.keywordAuthoraryl hydrocarbon receptor-
dc.subject.keywordAuthorCYP1A1-
dc.subject.keywordAuthorCYP1B1-
dc.subject.keywordAuthorquercetin-
dc.subject.keywordAuthormice-
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