File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus-pituitary-gonadal axis of CD-1 mice

TitleEffect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus-pituitary-gonadal axis of CD-1 mice
Authors
KeywordsGonadotrophin
GPR-54
Kisspeptin
Steroidogenesis
Issue Date2011
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/reprotox
Citation
Reproductive Toxicology, 2011, v. 31 n. 4, p. 409-417 How to Cite?
Abstract
Bisphenol A (BPA) is used in the manufacture of many products and is ubiquitous in the environment. Adverse effects of BPA on animal reproductive health have been reported, however most of the studies relied on the approaches in the assessment of conventional histology and anatomical features. The mechanistic actions of BPA are not clear. In the present study, a murine model was used to study potential effects of BPA exposure during perinatal and postnatal periods on endocrine functions of hypothalamic-pituitary-gonadal (HPG)-axis. At the hypothalamic-pituitary level, BPA exposure resulted in the up-regulation of the expression levels of KiSS-1, GnRH and FSH mRNA in both male and female pups. At the gonadal levels, BPA caused inhibition in the expressions of testicular steroidogenic enzymes and the synthesis of testosterone in the male pups. Conversely exposure to BPA resulted in a greater aromatase expression level and the synthesis of estrogen in the female pups. BPA is a weak estrogen agonist and its effects reported on animal studies are difficult to reconcile with mechanistic action of estrogen. In this study we hypothesized that the effects of BPA on reproductive dysfunction may be due to its actions on gonadal steroidogenesis and so the anomalous releases of endogenous steroid hormones. This non-ER-mediated effect is more potent in affecting the feedback regulatory circuits in the HPG-axis. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/139903
ISSN
2013 Impact Factor: 2.771
2013 SCImago Journal Rankings: 1.021
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Baptist University
University Grants CommitteeHKBU 1/CRF/08
Canada Research Chair program
Funding Information:

This work was supported by the Super Faculty Research Grant, Hong Kong Baptist University (CKC Wong) and Collaborative Research Fund (HKBU 1/CRF/08), University Grants Committee. Prof. Giesy was supported by the Canada Research Chair program and an at large Chair Professorship at the Department of Biology and Chemistry and State Key Laboratory in Marine Pollution, City University of Hong Kong.

References

 

Author Affiliations
  1. University of Saskatchewan
  2. The University of Hong Kong
  3. Hong Kong Baptist University
  4. City University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorXi, Wen_HK
dc.contributor.authorLee, CKFen_HK
dc.contributor.authorYeung, WSBen_HK
dc.contributor.authorGiesy, JPen_HK
dc.contributor.authorWong, MHen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorHecker, Men_HK
dc.contributor.authorWong, CKCen_HK
dc.date.accessioned2011-09-23T05:59:58Z-
dc.date.available2011-09-23T05:59:58Z-
dc.date.issued2011en_HK
dc.identifier.citationReproductive Toxicology, 2011, v. 31 n. 4, p. 409-417en_HK
dc.identifier.issn0890-6238en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139903-
dc.description.abstractBisphenol A (BPA) is used in the manufacture of many products and is ubiquitous in the environment. Adverse effects of BPA on animal reproductive health have been reported, however most of the studies relied on the approaches in the assessment of conventional histology and anatomical features. The mechanistic actions of BPA are not clear. In the present study, a murine model was used to study potential effects of BPA exposure during perinatal and postnatal periods on endocrine functions of hypothalamic-pituitary-gonadal (HPG)-axis. At the hypothalamic-pituitary level, BPA exposure resulted in the up-regulation of the expression levels of KiSS-1, GnRH and FSH mRNA in both male and female pups. At the gonadal levels, BPA caused inhibition in the expressions of testicular steroidogenic enzymes and the synthesis of testosterone in the male pups. Conversely exposure to BPA resulted in a greater aromatase expression level and the synthesis of estrogen in the female pups. BPA is a weak estrogen agonist and its effects reported on animal studies are difficult to reconcile with mechanistic action of estrogen. In this study we hypothesized that the effects of BPA on reproductive dysfunction may be due to its actions on gonadal steroidogenesis and so the anomalous releases of endogenous steroid hormones. This non-ER-mediated effect is more potent in affecting the feedback regulatory circuits in the HPG-axis. © 2010 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/reprotoxen_HK
dc.relation.ispartofReproductive Toxicologyen_HK
dc.subjectGonadotrophinen_HK
dc.subjectGPR-54en_HK
dc.subjectKisspeptinen_HK
dc.subjectSteroidogenesisen_HK
dc.subject.meshEndocrine Disruptors - toxicity-
dc.subject.meshEnvironmental Pollutants - toxicity-
dc.subject.meshHypothalamo-Hypophyseal System - drug effects - growth and development - metabolism-
dc.subject.meshOvary - drug effects - growth and development - metabolism-
dc.subject.meshTestis - drug effects - growth and development - metabolism-
dc.titleEffect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus-pituitary-gonadal axis of CD-1 miceen_HK
dc.typeArticleen_HK
dc.identifier.emailYeung, WSB:wsbyeung@hkucc.hku.hken_HK
dc.identifier.authorityYeung, WSB=rp00331en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.reprotox.2010.12.002en_HK
dc.identifier.pmid21182934en_HK
dc.identifier.scopuseid_2-s2.0-79956370282en_HK
dc.identifier.hkuros196016en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79956370282&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue4en_HK
dc.identifier.spage409en_HK
dc.identifier.epage417en_HK
dc.identifier.isiWOS:000291377200005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXi, W=52164751400en_HK
dc.identifier.scopusauthoridLee, CKF=8757364600en_HK
dc.identifier.scopusauthoridYeung, WSB=7102370745en_HK
dc.identifier.scopusauthoridGiesy, JP=35459135300en_HK
dc.identifier.scopusauthoridWong, MH=7403908633en_HK
dc.identifier.scopusauthoridZhang, X=36086912900en_HK
dc.identifier.scopusauthoridHecker, M=35247848500en_HK
dc.identifier.scopusauthoridWong, CKC=35276549400en_HK
dc.identifier.citeulike8611783-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats