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Article: Modulation of steroidogenic gene expression and hormone synthesis in H295R cells exposed to PCP and TCP
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TitleModulation of steroidogenic gene expression and hormone synthesis in H295R cells exposed to PCP and TCP
 
AuthorsMa, Y6 1
Liu, C6
Lam, PKS7
Wu, RSS4
Giesy, JP2 7 4 3 5
Hecker, M2
Zhang, X2
Zhou, B6
 
KeywordsCAMP
Chlorophenol
Endocrine-disruption
Gene expression
H295R
Steroid hormone
 
Issue Date2011
 
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
 
CitationToxicology, 2011, v. 282 n. 3, p. 146-153 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.tox.2011.01.024
 
AbstractChlorophenols (CPs) have been suspected to disrupt the endocrine system and thus affect human and wildlife reproduction but less is known about the underlying mechanism. In this study, we investigated the effects of pentachlorophenol (PCP) and 2,4,6-trichlorophenol (TCP) on human adrenocortical carcinoma cell line (H295R). The H295R cells were exposed to environmentally relevant concentration (0.0, 0.4, 1.1, 3.4 μM) of PCP and TCP for 48. h, and expression of specific genes involved in steroidogenesis, including cytochrome P450 (CYP11A, CYP17, CYP19), 3βHSD2, 17βHSD4 and StAR was quantitatively measured using real-time polymerase chain reaction. The selected gene expressions were significantly down-regulated compared with those in the control group. Exposure to PCP and TCP significantly decreased production of both testosterone (T) and 17β-estradiol (E2). Furthermore, a dose-dependent decrease of cellular cAMP was observed in H295R cells exposed to both PCP and TCP. A time-course study revealed that the observed selected steroidogenic gene expressions and protein abundance (StAR) are consistent with reduced cellular cAMP concentrations. The results showed that PCP and TCP may inhibit steroidogenesis by disrupting cAMP signaling. The research indicates that H295R cells can be used as an in vitro model for endocrine disruption assay for chlorophenols and the mechanism involvement of disturbing cAMP signaling. © 2011 Elsevier Ireland Ltd.
 
ISSN0300-483X
2012 Impact Factor: 4.017
2012 SCImago Journal Rankings: 1.094
 
DOIhttp://dx.doi.org/10.1016/j.tox.2011.01.024
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorMa, Y
 
dc.contributor.authorLiu, C
 
dc.contributor.authorLam, PKS
 
dc.contributor.authorWu, RSS
 
dc.contributor.authorGiesy, JP
 
dc.contributor.authorHecker, M
 
dc.contributor.authorZhang, X
 
dc.contributor.authorZhou, B
 
dc.date.accessioned2012-09-20T08:25:46Z
 
dc.date.available2012-09-20T08:25:46Z
 
dc.date.issued2011
 
dc.description.abstractChlorophenols (CPs) have been suspected to disrupt the endocrine system and thus affect human and wildlife reproduction but less is known about the underlying mechanism. In this study, we investigated the effects of pentachlorophenol (PCP) and 2,4,6-trichlorophenol (TCP) on human adrenocortical carcinoma cell line (H295R). The H295R cells were exposed to environmentally relevant concentration (0.0, 0.4, 1.1, 3.4 μM) of PCP and TCP for 48. h, and expression of specific genes involved in steroidogenesis, including cytochrome P450 (CYP11A, CYP17, CYP19), 3βHSD2, 17βHSD4 and StAR was quantitatively measured using real-time polymerase chain reaction. The selected gene expressions were significantly down-regulated compared with those in the control group. Exposure to PCP and TCP significantly decreased production of both testosterone (T) and 17β-estradiol (E2). Furthermore, a dose-dependent decrease of cellular cAMP was observed in H295R cells exposed to both PCP and TCP. A time-course study revealed that the observed selected steroidogenic gene expressions and protein abundance (StAR) are consistent with reduced cellular cAMP concentrations. The results showed that PCP and TCP may inhibit steroidogenesis by disrupting cAMP signaling. The research indicates that H295R cells can be used as an in vitro model for endocrine disruption assay for chlorophenols and the mechanism involvement of disturbing cAMP signaling. © 2011 Elsevier Ireland Ltd.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationToxicology, 2011, v. 282 n. 3, p. 146-153 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.tox.2011.01.024
 
dc.identifier.citeulike8795310
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.tox.2011.01.024
 
dc.identifier.epage153
 
dc.identifier.hkuros208998
 
dc.identifier.issn0300-483X
2012 Impact Factor: 4.017
2012 SCImago Journal Rankings: 1.094
 
dc.identifier.issue3
 
dc.identifier.pmid21296122
 
dc.identifier.scopuseid_2-s2.0-79952310970
 
dc.identifier.spage146
 
dc.identifier.urihttp://hdl.handle.net/10722/165950
 
dc.identifier.volume282
 
dc.languageeng
 
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
 
dc.publisher.placeIreland
 
dc.relation.ispartofToxicology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshChlorophenols - toxicity
 
dc.subject.meshEndocrine Disruptors - toxicity
 
dc.subject.meshGene Expression Regulation - drug effects
 
dc.subject.meshGonadal Steroid Hormones - biosynthesis - genetics
 
dc.subject.meshPentachlorophenol - toxicity
 
dc.subjectCAMP
 
dc.subjectChlorophenol
 
dc.subjectEndocrine-disruption
 
dc.subjectGene expression
 
dc.subjectH295R
 
dc.subjectSteroid hormone
 
dc.titleModulation of steroidogenic gene expression and hormone synthesis in H295R cells exposed to PCP and TCP
 
dc.typeArticle
 
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<contributor.author>Giesy, JP</contributor.author>
<contributor.author>Hecker, M</contributor.author>
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Author Affiliations
  1. Graduate University of Chinese Academy of Sciences
  2. University of Saskatchewan
  3. King Saud University College of Science
  4. The University of Hong Kong
  5. Michigan State University
  6. Institute of Hydrobiology, Chinese Academy of Sciences
  7. City University of Hong Kong