File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1093/toxsci/kfh045
- Scopus: eid_2-s2.0-1542686227
- PMID: 14691211
- WOS: WOS:000220076000006
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Modulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cells
Title | Modulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cells |
---|---|
Authors | |
Keywords | 17β-estradiol CYP1A1 mRNA Dexamethasone EROD H411E cells |
Issue Date | 2004 |
Publisher | Oxford 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? |
Abstract | TCDD 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 Identifier | http://hdl.handle.net/10722/183392 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 0.911 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lai, KP | en_US |
dc.contributor.author | Wong, MH | en_US |
dc.contributor.author | Wong, CKC | en_US |
dc.date.accessioned | 2013-05-27T07:12:30Z | - |
dc.date.available | 2013-05-27T07:12:30Z | - |
dc.date.issued | 2004 | en_US |
dc.identifier.citation | Toxicological Sciences, 2004, v. 78 n. 1, p. 41-49 | en_US |
dc.identifier.issn | 1096-6080 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/183392 | - |
dc.description.abstract | TCDD 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.language | eng | en_US |
dc.publisher | Oxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/ | en_US |
dc.relation.ispartof | Toxicological Sciences | en_US |
dc.subject | 17β-estradiol | - |
dc.subject | CYP1A1 mRNA | - |
dc.subject | Dexamethasone | - |
dc.subject | EROD | - |
dc.subject | H411E cells | - |
dc.subject.mesh | Actins - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anti-Inflammatory Agents, Non-Steroidal - Pharmacology | en_US |
dc.subject.mesh | Blotting, Western | en_US |
dc.subject.mesh | Cell Line, Tumor | en_US |
dc.subject.mesh | Cycloheximide - Pharmacology | en_US |
dc.subject.mesh | Cytochrome P-450 Cyp1a1 - Biosynthesis | en_US |
dc.subject.mesh | Dna Primers | en_US |
dc.subject.mesh | Dexamethasone - Pharmacology | en_US |
dc.subject.mesh | Environmental Pollutants - Toxicity | en_US |
dc.subject.mesh | Estradiol - Pharmacology | en_US |
dc.subject.mesh | Gene Expression Regulation, Enzymologic - Drug Effects | en_US |
dc.subject.mesh | Hormones - Pharmacology | en_US |
dc.subject.mesh | Liver Neoplasms, Experimental - Enzymology - Metabolism | en_US |
dc.subject.mesh | Protein Processing, Post-Translational - Physiology | en_US |
dc.subject.mesh | Protein Synthesis Inhibitors - Pharmacology | en_US |
dc.subject.mesh | Rna, Messenger - Metabolism | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Receptors, Aryl Hydrocarbon - Metabolism | en_US |
dc.subject.mesh | Reverse Transcriptase Polymerase Chain Reaction | en_US |
dc.subject.mesh | Tetrachlorodibenzodioxin - Toxicity | en_US |
dc.title | Modulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17β-estradiol and dexamethasone in TCDD-induced H411E cells | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lai, KP: ballllai@hotmail.com | en_US |
dc.identifier.authority | Lai, KP=rp01753 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1093/toxsci/kfh045 | en_US |
dc.identifier.pmid | 14691211 | - |
dc.identifier.scopus | eid_2-s2.0-1542686227 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-1542686227&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 78 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 41 | en_US |
dc.identifier.epage | 49 | en_US |
dc.identifier.isi | WOS:000220076000006 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Lai, KP=7402135707 | en_US |
dc.identifier.scopusauthorid | Wong, MH=7403908633 | en_US |
dc.identifier.scopusauthorid | Wong, CKC=35276549400 | en_US |
dc.identifier.issnl | 1096-0929 | - |