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Article: Effects of brominated flame retardants and brominated dioxins on steroidogenesis in H295R human adrenocortical carcinoma cell line

TitleEffects of brominated flame retardants and brominated dioxins on steroidogenesis in H295R human adrenocortical carcinoma cell line
Authors
KeywordsBrominated flame retardants
Bromodioxins
Gene expression
H295R
Steroidogenesis
Issue Date2007
PublisherSociety of Environmental Toxicology and Chemistry. The Journal's web site is located at http://etc.allenpress.com/
Citation
Environmental Toxicology And Chemistry, 2007, v. 26 n. 4, p. 764-772 How to Cite?
AbstractBrominated flame retardants (BFRs) and brominated dioxins are emerging persistent organic pollutants that are ubiquitous in the environment and can be accumulated by wildlife and humans. These chemicals can disturb endocrine function. Recent studies have demonstrated that one of the mechanisms of endocrine disruption by chemicals is modulation of steroidogenic gene expression or enzyme activities. In this study, an in vitro assay based on the H295R human adrenocortical carcinoma cell line, which possesses most key genes or enzymes involved in steroidogenesis, was used to examine the effects of five bromophenols, two polybrominated biphenyls (PBBs 77 and 169), 2,3,7,8-tetrabromodibenzo-p-dioxin, and 2,3,7,8-tetrabromodibenzofuran on the expression of 10 key steroidogenic genes. The H295R cells were exposed to various BFR concentrations for 48 h, and the expression of specific genes - cytochrome P450 (CYP11A, CYP11B2, CYP17, CYP19, and CYP21), 3β- hydroxysteroid dehydrogenase (3βHSD2), 17β-hydroxysteroid dehydrogenase (17βHSD1 and 17βHSD4), steroidogenic acute regulatory protein (StAR), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) - was quantitatively measured using real-time polymerase chain reaction. Cell viability was not affected at the doses tested. Most of the genes were either up- or down-regulated, to some extent, by BFR exposure. Among the genes tested, 3βHSD2 was the most markedly up-regulated, with a range of magnitude from 1.6- to 20-fold. The results demonstrate that bromophenol, bromobiphenyls, and bromodibenzo-p-dioxin/furan are able to modulate steroidogenic gene expression, which may lead to endocrine disruption. © 2007 SETAC.
Persistent Identifierhttp://hdl.handle.net/10722/178995
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.268
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDing, Len_US
dc.contributor.authorMurphy, MBen_US
dc.contributor.authorHe, Yen_US
dc.contributor.authorXu, Yen_US
dc.contributor.authorYeung, LWYen_US
dc.contributor.authorWang, Jen_US
dc.contributor.authorZhou, Ben_US
dc.contributor.authorLam, PKSen_US
dc.contributor.authorWu, RSSen_US
dc.contributor.authorGiesy, JPen_US
dc.date.accessioned2012-12-19T09:51:18Z-
dc.date.available2012-12-19T09:51:18Z-
dc.date.issued2007en_US
dc.identifier.citationEnvironmental Toxicology And Chemistry, 2007, v. 26 n. 4, p. 764-772en_US
dc.identifier.issn0730-7268en_US
dc.identifier.urihttp://hdl.handle.net/10722/178995-
dc.description.abstractBrominated flame retardants (BFRs) and brominated dioxins are emerging persistent organic pollutants that are ubiquitous in the environment and can be accumulated by wildlife and humans. These chemicals can disturb endocrine function. Recent studies have demonstrated that one of the mechanisms of endocrine disruption by chemicals is modulation of steroidogenic gene expression or enzyme activities. In this study, an in vitro assay based on the H295R human adrenocortical carcinoma cell line, which possesses most key genes or enzymes involved in steroidogenesis, was used to examine the effects of five bromophenols, two polybrominated biphenyls (PBBs 77 and 169), 2,3,7,8-tetrabromodibenzo-p-dioxin, and 2,3,7,8-tetrabromodibenzofuran on the expression of 10 key steroidogenic genes. The H295R cells were exposed to various BFR concentrations for 48 h, and the expression of specific genes - cytochrome P450 (CYP11A, CYP11B2, CYP17, CYP19, and CYP21), 3β- hydroxysteroid dehydrogenase (3βHSD2), 17β-hydroxysteroid dehydrogenase (17βHSD1 and 17βHSD4), steroidogenic acute regulatory protein (StAR), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) - was quantitatively measured using real-time polymerase chain reaction. Cell viability was not affected at the doses tested. Most of the genes were either up- or down-regulated, to some extent, by BFR exposure. Among the genes tested, 3βHSD2 was the most markedly up-regulated, with a range of magnitude from 1.6- to 20-fold. The results demonstrate that bromophenol, bromobiphenyls, and bromodibenzo-p-dioxin/furan are able to modulate steroidogenic gene expression, which may lead to endocrine disruption. © 2007 SETAC.en_US
dc.languageengen_US
dc.publisherSociety of Environmental Toxicology and Chemistry. The Journal's web site is located at http://etc.allenpress.com/en_US
dc.relation.ispartofEnvironmental Toxicology and Chemistryen_US
dc.subjectBrominated flame retardants-
dc.subjectBromodioxins-
dc.subjectGene expression-
dc.subjectH295R-
dc.subjectSteroidogenesis-
dc.subject.mesh17-Hydroxysteroid Dehydrogenases - Metabolismen_US
dc.subject.mesh3-Hydroxysteroid Dehydrogenases - Metabolismen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCytochrome P-450 Enzyme System - Metabolismen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDna, Complementary - Geneticsen_US
dc.subject.meshDioxins - Toxicityen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshFlame Retardants - Toxicityen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshHydrocarbons, Brominated - Toxicityen_US
dc.subject.meshHydroxymethylglutaryl Coa Reductases - Metabolismen_US
dc.subject.meshPhosphoproteins - Metabolismen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshSteroids - Biosynthesisen_US
dc.titleEffects of brominated flame retardants and brominated dioxins on steroidogenesis in H295R human adrenocortical carcinoma cell lineen_US
dc.typeArticleen_US
dc.identifier.emailWu, RSS: rudolfwu@hku.hken_US
dc.identifier.authorityWu, RSS=rp01398en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1897/06-388R1.1en_US
dc.identifier.pmid17447562-
dc.identifier.scopuseid_2-s2.0-34247530702en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247530702&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume26en_US
dc.identifier.issue4en_US
dc.identifier.spage764en_US
dc.identifier.epage772en_US
dc.identifier.isiWOS:000244938200023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDing, L=55144466700en_US
dc.identifier.scopusauthoridMurphy, MB=7403900446en_US
dc.identifier.scopusauthoridHe, Y=16241582000en_US
dc.identifier.scopusauthoridXu, Y=7406447917en_US
dc.identifier.scopusauthoridYeung, LWY=9735175200en_US
dc.identifier.scopusauthoridWang, J=8941425500en_US
dc.identifier.scopusauthoridZhou, B=7401906781en_US
dc.identifier.scopusauthoridLam, PKS=7202365776en_US
dc.identifier.scopusauthoridWu, RSS=7402945079en_US
dc.identifier.scopusauthoridGiesy, JP=35459135300en_US
dc.identifier.issnl0730-7268-

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