File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Disruption of the blood-testis barrier integrity by bisphenol A in vitro: Is this a suitable model for studying blood-testis barrier dynamics?

TitleDisruption of the blood-testis barrier integrity by bisphenol A in vitro: Is this a suitable model for studying blood-testis barrier dynamics?
Authors
KeywordsAnchoring junction
Bisphenol A
Seminiferous epithelial cycle
Sertoli cells
Spermatogenesis
Testis
Tight junction
Issue Date2009
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocel
Citation
International Journal Of Biochemistry And Cell Biology, 2009, v. 41 n. 11, p. 2302-2314 How to Cite?
AbstractBisphenol A, an estrogenic environmental toxicant, has been implicated to have hazardous effects on reproductive health in humans and rodents. However, there are conflicting reports in the literature regarding its effects on male reproductive function. In this study, it was shown that in adult rats treated with acute doses of bisphenol A, a small but statistically insignificant percentage of seminiferous tubules in the testes displayed signs of germ cell loss, consistent with some earlier reports. It also failed to disrupt the blood-testis barrier in vivo. This is possibly due to the low bioavailability of free bisphenol A in the systemic circulation. However, bisphenol A disrupted the blood-testis barrier when administered to immature 20-day-old rats, consistent with earlier reports concerning the higher susceptibility of immature rats towards bisphenol A. This observation was confirmed using primary Sertoli cells cultured in vitro with established tight junction-permeability barrier that mimicked the blood-testis barrier in vivo. The reversible disruption of Sertoli cell tight junction barrier by bisphenol A was associated with an activation of ERK, and a decline in the levels of selected proteins at the tight junction, basal ectoplasmic specialization, and gap junction at the blood-testis barrier. Studies by dual-labeled immunofluorescence analysis and biotinylation techniques also illustrated declining levels of occludin, connexin 43, and N-cadherin at the cell-cell interface following bisphenol A treatment. In summary, bisphenol A reversibly perturbs the integrity of the blood-testis barrier in Sertoli cells in vitro, which can also serve as a suitable model for studying the dynamics of the blood-testis barrier. © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/127439
ISSN
2015 Impact Factor: 3.905
2015 SCImago Journal Rankings: 2.003
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, MWMen_HK
dc.contributor.authorMruk, DDen_HK
dc.contributor.authorLee, WMen_HK
dc.contributor.authorCheng, CYen_HK
dc.date.accessioned2010-10-31T13:25:39Z-
dc.date.available2010-10-31T13:25:39Z-
dc.date.issued2009en_HK
dc.identifier.citationInternational Journal Of Biochemistry And Cell Biology, 2009, v. 41 n. 11, p. 2302-2314en_HK
dc.identifier.issn1357-2725en_HK
dc.identifier.urihttp://hdl.handle.net/10722/127439-
dc.description.abstractBisphenol A, an estrogenic environmental toxicant, has been implicated to have hazardous effects on reproductive health in humans and rodents. However, there are conflicting reports in the literature regarding its effects on male reproductive function. In this study, it was shown that in adult rats treated with acute doses of bisphenol A, a small but statistically insignificant percentage of seminiferous tubules in the testes displayed signs of germ cell loss, consistent with some earlier reports. It also failed to disrupt the blood-testis barrier in vivo. This is possibly due to the low bioavailability of free bisphenol A in the systemic circulation. However, bisphenol A disrupted the blood-testis barrier when administered to immature 20-day-old rats, consistent with earlier reports concerning the higher susceptibility of immature rats towards bisphenol A. This observation was confirmed using primary Sertoli cells cultured in vitro with established tight junction-permeability barrier that mimicked the blood-testis barrier in vivo. The reversible disruption of Sertoli cell tight junction barrier by bisphenol A was associated with an activation of ERK, and a decline in the levels of selected proteins at the tight junction, basal ectoplasmic specialization, and gap junction at the blood-testis barrier. Studies by dual-labeled immunofluorescence analysis and biotinylation techniques also illustrated declining levels of occludin, connexin 43, and N-cadherin at the cell-cell interface following bisphenol A treatment. In summary, bisphenol A reversibly perturbs the integrity of the blood-testis barrier in Sertoli cells in vitro, which can also serve as a suitable model for studying the dynamics of the blood-testis barrier. © 2009 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocelen_HK
dc.relation.ispartofInternational Journal of Biochemistry and Cell Biologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAnchoring junctionen_HK
dc.subjectBisphenol Aen_HK
dc.subjectSeminiferous epithelial cycleen_HK
dc.subjectSertoli cellsen_HK
dc.subjectSpermatogenesisen_HK
dc.subjectTestisen_HK
dc.subjectTight junctionen_HK
dc.subject.meshAging - drug effects - pathology-
dc.subject.meshAnimals-
dc.subject.meshBlood-Testis Barrier - drug effects - pathology - ultrastructure-
dc.subject.meshModels, Biological-
dc.subject.meshPhenols - toxicity-
dc.titleDisruption of the blood-testis barrier integrity by bisphenol A in vitro: Is this a suitable model for studying blood-testis barrier dynamics?en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1357-2725&volume=41&issue=11&spage=2302&epage=2314&date=2009&atitle=Disruption+of+the+blood-testis+barrier+integrity+by+bisphenol+A+in+vitro:+Is+this+a+suitable+model+for+studying+blood-testis+barrier+dynamics?-
dc.identifier.emailLee, WM: hrszlwm@hku.hken_HK
dc.identifier.authorityLee, WM=rp00728en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.biocel.2009.05.016en_HK
dc.identifier.pmid19497385-
dc.identifier.scopuseid_2-s2.0-69249232433en_HK
dc.identifier.hkuros179020en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-69249232433&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume41en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2302en_HK
dc.identifier.epage2314en_HK
dc.identifier.isiWOS:000271124700027-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLi, MWM=27168276300en_HK
dc.identifier.scopusauthoridMruk, DD=6701823934en_HK
dc.identifier.scopusauthoridLee, WM=24799156600en_HK
dc.identifier.scopusauthoridCheng, CY=7404797787en_HK
dc.identifier.citeulike5240932-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats