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Article: Modulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cells

TitleModulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cells
Authors
Issue Date2004
PublisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/
Citation
Toxicological Sciences, 2004, v. 78 n. 1, p. 41-49 How to Cite?
AbstractTCDD elicits a variety of species- and organ-specific pathological consequences. The differential toxicities are thought to relate to the de novo modulation of TCDD action by endogenous hormones. Previous studies from this laboratory demonstrated a dose-and time-dependent induction of CYP1A1 expression and 7-ethoxyresorufin-O-deethylase (EROD) activities in H4IIE cells by picomolar levels of TCDD treatment. In this study, we examined the hormonal modulation of TCDD-elicited AhR-mediated biochemical responses. Lipid-soluble hormones, 17β-estradiol (E2), diethylstilbestrol (DES), testosterone (T), 5α-dihydrotestosterone (DHT), dexamethasone (DEX), and T3 were studied for their possible interactions with the TCDD-mediated effects. Our results showed that CYP1A1 expression and EROD activities induced by TCDD were potentiated or suppressed, respectively, by DEX or E2/DES treatment. Other tested hormones, however, had no significant effect. Using a receptor antagonist (RU486), DEX-mediated potentiation of TCDD-elicited EROD activity was completely abolished. E2-mediated suppression, however, was not affected by cotreatment with the estrogen receptor antagonists, 4-hydroxytamoxifen or ICI 182780. Taking a step further to dissect the possible mechanisms involved, with the aid of cycloheximide (CHX), DEX-mediated potentiation was found to depend on the posttranscriptional process. The DEX pretreatment study indicated that the potentiation was a time-dependent process. In contrast, E2-mediated suppression did not rely on the synthesis of protein factors. Presumably it might hinder the formation of the activated TCDD/AhR complex and so the subsequent binding on DRE. © Society of Toxicology 2004; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/183392
ISSN
2015 Impact Factor: 3.88
2015 SCImago Journal Rankings: 1.686
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KPen_US
dc.contributor.authorWong, MHen_US
dc.contributor.authorWong, CKCen_US
dc.date.accessioned2013-05-27T07:12:30Z-
dc.date.available2013-05-27T07:12:30Z-
dc.date.issued2004en_US
dc.identifier.citationToxicological Sciences, 2004, v. 78 n. 1, p. 41-49en_US
dc.identifier.issn1096-6080en_US
dc.identifier.urihttp://hdl.handle.net/10722/183392-
dc.description.abstractTCDD elicits a variety of species- and organ-specific pathological consequences. The differential toxicities are thought to relate to the de novo modulation of TCDD action by endogenous hormones. Previous studies from this laboratory demonstrated a dose-and time-dependent induction of CYP1A1 expression and 7-ethoxyresorufin-O-deethylase (EROD) activities in H4IIE cells by picomolar levels of TCDD treatment. In this study, we examined the hormonal modulation of TCDD-elicited AhR-mediated biochemical responses. Lipid-soluble hormones, 17β-estradiol (E2), diethylstilbestrol (DES), testosterone (T), 5α-dihydrotestosterone (DHT), dexamethasone (DEX), and T3 were studied for their possible interactions with the TCDD-mediated effects. Our results showed that CYP1A1 expression and EROD activities induced by TCDD were potentiated or suppressed, respectively, by DEX or E2/DES treatment. Other tested hormones, however, had no significant effect. Using a receptor antagonist (RU486), DEX-mediated potentiation of TCDD-elicited EROD activity was completely abolished. E2-mediated suppression, however, was not affected by cotreatment with the estrogen receptor antagonists, 4-hydroxytamoxifen or ICI 182780. Taking a step further to dissect the possible mechanisms involved, with the aid of cycloheximide (CHX), DEX-mediated potentiation was found to depend on the posttranscriptional process. The DEX pretreatment study indicated that the potentiation was a time-dependent process. In contrast, E2-mediated suppression did not rely on the synthesis of protein factors. Presumably it might hinder the formation of the activated TCDD/AhR complex and so the subsequent binding on DRE. © Society of Toxicology 2004; all rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/en_US
dc.relation.ispartofToxicological Sciencesen_US
dc.subject.meshActins - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Pharmacologyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCycloheximide - Pharmacologyen_US
dc.subject.meshCytochrome P-450 Cyp1a1 - Biosynthesisen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshEnvironmental Pollutants - Toxicityen_US
dc.subject.meshEstradiol - Pharmacologyen_US
dc.subject.meshGene Expression Regulation, Enzymologic - Drug Effectsen_US
dc.subject.meshHormones - Pharmacologyen_US
dc.subject.meshLiver Neoplasms, Experimental - Enzymology - Metabolismen_US
dc.subject.meshProtein Processing, Post-Translational - Physiologyen_US
dc.subject.meshProtein Synthesis Inhibitors - Pharmacologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, Aryl Hydrocarbon - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTetrachlorodibenzodioxin - Toxicityen_US
dc.titleModulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cellsen_US
dc.typeArticleen_US
dc.identifier.emailLai, KP: ballllai@hotmail.comen_US
dc.identifier.authorityLai, KP=rp01753en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/toxsci/kfh045en_US
dc.identifier.pmid14691211-
dc.identifier.scopuseid_2-s2.0-1542686227en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1542686227&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume78en_US
dc.identifier.issue1en_US
dc.identifier.spage41en_US
dc.identifier.epage49en_US
dc.identifier.isiWOS:000220076000006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLai, KP=7402135707en_US
dc.identifier.scopusauthoridWong, MH=7403908633en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US

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