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Article: Estrogenic phenol and catechol metabolites of PCBs modulate catechol-o-methyltransferase expression via the estrogen receptor: Potential contribution to cancer risk

TitleEstrogenic phenol and catechol metabolites of PCBs modulate catechol-o-methyltransferase expression via the estrogen receptor: Potential contribution to cancer risk
Authors
KeywordsCarcinogenesis
COMT
Estrogen
PCB
Xenobiotic catechols
Issue Date2008
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cdm/index.htm
Citation
Current Drug Metabolism, 2008, v. 9 n. 4, p. 304-309 How to Cite?
AbstractCommercial PCB mixtures have been shown to induce liver tumors in female rats and this effect has been attributed to the effects of PCBs on estrogen metabolism. Catechol metabolites of PCBs are potent inhibitors of COMT activity and are likely to contribute significantly to reduced clearance of genotoxic catechol metabolites of estrogen. The effect of PCB metabolites on COMT expression in cultured cells was investigated to explore potential mechanisms by which PCB exposure alters catechol estrogen clearance. We hypothesize that estrogenic PCB metabolites may contribute to reduction of COMT expression via interaction with the estrogen receptor. To test this hypothesis, human MCF-7 cells were exposed to PCB analogues and the expression of COMT determined. Western blot analysis demonstrated that COMT protein levels were statistically significantly reduced by both the phenolic and the catechol compounds, an effect which was abolished by the anti-estrogen, ICI182780. The above suggests that COMT levels may be reduced by estrogenic PCB metabolites, via interactions between PCB metabolites and the ER. It supports the hypothesis that both phenolic and catechol metabolites of PCBs may contribute to PCB-mediated carcinogenesis through reduction of COMT levels and activities and subsequent reduction in clearance of endogenous and xenobiotic catechols. © 2008 Bentham Science Publishers Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/78741
ISSN
2015 Impact Factor: 2.847
2015 SCImago Journal Rankings: 0.976
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, PWLen_HK
dc.contributor.authorGarner, CEen_HK
dc.contributor.authorHo, JWMen_HK
dc.contributor.authorLeung, KCen_HK
dc.contributor.authorChu, ACYen_HK
dc.contributor.authorKwok, KHHen_HK
dc.contributor.authorKung, MHWen_HK
dc.contributor.authorBurka, LTen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2010-09-06T07:46:13Z-
dc.date.available2010-09-06T07:46:13Z-
dc.date.issued2008en_HK
dc.identifier.citationCurrent Drug Metabolism, 2008, v. 9 n. 4, p. 304-309en_HK
dc.identifier.issn1389-2002en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78741-
dc.description.abstractCommercial PCB mixtures have been shown to induce liver tumors in female rats and this effect has been attributed to the effects of PCBs on estrogen metabolism. Catechol metabolites of PCBs are potent inhibitors of COMT activity and are likely to contribute significantly to reduced clearance of genotoxic catechol metabolites of estrogen. The effect of PCB metabolites on COMT expression in cultured cells was investigated to explore potential mechanisms by which PCB exposure alters catechol estrogen clearance. We hypothesize that estrogenic PCB metabolites may contribute to reduction of COMT expression via interaction with the estrogen receptor. To test this hypothesis, human MCF-7 cells were exposed to PCB analogues and the expression of COMT determined. Western blot analysis demonstrated that COMT protein levels were statistically significantly reduced by both the phenolic and the catechol compounds, an effect which was abolished by the anti-estrogen, ICI182780. The above suggests that COMT levels may be reduced by estrogenic PCB metabolites, via interactions between PCB metabolites and the ER. It supports the hypothesis that both phenolic and catechol metabolites of PCBs may contribute to PCB-mediated carcinogenesis through reduction of COMT levels and activities and subsequent reduction in clearance of endogenous and xenobiotic catechols. © 2008 Bentham Science Publishers Ltd.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cdm/index.htmen_HK
dc.relation.ispartofCurrent Drug Metabolismen_HK
dc.subjectCarcinogenesisen_HK
dc.subjectCOMTen_HK
dc.subjectEstrogenen_HK
dc.subjectPCBen_HK
dc.subjectXenobiotic catecholsen_HK
dc.subject.meshActins - toxicityen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCatechol O-Methyltransferase - biosynthesisen_HK
dc.subject.meshCatechols - metabolism - pharmacology - toxicityen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshElectrophoresis, Polyacrylamide Gelen_HK
dc.subject.meshEnvironmental Pollutants - metabolism - pharmacology - toxicityen_HK
dc.subject.meshEstradiol - analogs & derivatives - pharmacologyen_HK
dc.subject.meshEstrogen Antagonists - pharmacologyen_HK
dc.subject.meshEstrogens, Non-Steroidalen_HK
dc.subject.meshHumansen_HK
dc.subject.meshNeoplasms - chemically induced - epidemiologyen_HK
dc.subject.meshPhenols - metabolism - pharmacology - toxicityen_HK
dc.subject.meshPolychlorinated Biphenyls - metabolism - pharmacology - toxicityen_HK
dc.subject.meshReceptors, Estrogen - drug effectsen_HK
dc.subject.meshRisken_HK
dc.titleEstrogenic phenol and catechol metabolites of PCBs modulate catechol-o-methyltransferase expression via the estrogen receptor: Potential contribution to cancer risken_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1389-2002&volume=9&issue=4&spage=304&epage=309&date=2008&atitle=Estrogenic+phenol+and+catechol+metabolites+of+PCBs+modulate+catechol-O-methyltransferase+expression+via+the+estrogen+receptor:+potential+contribution+to+cancer+risk.en_HK
dc.identifier.emailHo, PWL: hwl2002@hku.hken_HK
dc.identifier.emailChu, ACY: bcccy@hkucc.hku.hken_HK
dc.identifier.emailHo, SL: slho@hku.hken_HK
dc.identifier.authorityHo, PWL=rp00259en_HK
dc.identifier.authorityChu, ACY=rp00505en_HK
dc.identifier.authorityHo, SL=rp00240en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/138920008784220600en_HK
dc.identifier.pmid18473748-
dc.identifier.scopuseid_2-s2.0-45249092256en_HK
dc.identifier.hkuros142948en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-45249092256&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue4en_HK
dc.identifier.spage304en_HK
dc.identifier.epage309en_HK
dc.identifier.isiWOS:000255682300006-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridHo, PWL=25027612100en_HK
dc.identifier.scopusauthoridGarner, CE=7202557436en_HK
dc.identifier.scopusauthoridHo, JWM=8685214100en_HK
dc.identifier.scopusauthoridLeung, KC=7401860725en_HK
dc.identifier.scopusauthoridChu, ACY=24343085700en_HK
dc.identifier.scopusauthoridKwok, KHH=7102194193en_HK
dc.identifier.scopusauthoridKung, MHW=36336960300en_HK
dc.identifier.scopusauthoridBurka, LT=7004566763en_HK
dc.identifier.scopusauthoridRamsden, DB=7102612805en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK
dc.identifier.citeulike2750294-

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