Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate

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dc.contributor.authorMahood, K.
dc.contributor.authorMcKinnell, C.
dc.contributor.authorWalker, M.
dc.contributor.authorHallmark, N.
dc.contributor.authorScott, H.
dc.contributor.authorFisher, J.
dc.contributor.authorRivas, A.
dc.contributor.authorHartung, S.
dc.contributor.authorIvell, R.
dc.contributor.authorMason, J.
dc.contributor.authorSharpe, R.
dc.date.issued2006
dc.descriptionThe definitive version is available at www.blackwell-synergy.com
dc.description.abstractFoetal exposure of male rats to di(n-butyl) phthalate (DBP) induces testicular changes similar to testicular dysgenesis syndrome in humans, including the formation of focal 'dysgenetic areas' within post-natal testes, surrounded by otherwise normal tubules exhibiting complete spermatogenesis. We hypothesize that these dysgenetic areas form when Sertoli (and other) cells are 'trapped' during the abnormal formation of large Leydig cell (LC) clusters in foetal life and by post-natal day (d) 4 these groups of intermingled cells attempt to form seminiferous tubules. It is likely that the malformed tubules resulting correspond to the dysgenetic areas evident in later life. This also provides a plausible explanation for the occurrence of LCs within seminiferous cords/tubules in or bordering the dysgenetic areas. In our previous studies intratubular LCs (ITLCs) were identified by immunostaining for 3beta-hydroxysteroid dehydrogenase (3beta-HSD), the definitive LC cytoplasmic marker. However, the possibility remained that the 'presumptive' ITLCs were in fact Sertoli cells that had aberrantly gained the ability to express 3beta-HSD. Therefore, the aim of the present study was to fully characterize the ITLCs induced by in utero DBP exposure in d25 rats using a number of LC- (3beta-HSD, P450 side-chain cleavage enzyme, insulin-like factor 3, oestrogen receptor alpha) and Sertoli cell- (vimentin, Wilm's tumour-1) specific markers. Our results show that ITLCs express all four LC-specific markers but do not express either of the Sertoli cell markers. It is therefore concluded that the ITLCs are bona fide LCs that are abnormally located within the seminiferous tubules of DBP-exposed rats in post-natal life.
dc.description.statementofresponsibilityI. Kim Mahood, Chris McKinnell, Marion Walker, Nina Hallmark, Hayley Scott, Jane S. Fisher, Ana Rivas, Stefan Hartung, Richard Ivell, J. Ian Mason, and Richard M. Sharpe
dc.identifier.citationInternational Journal of Andrology, 2006; 29(1):148-153
dc.identifier.doi10.1111/j.1365-2605.2005.00574.x
dc.identifier.issn0105-6263
dc.identifier.issn1365-2605
dc.identifier.urihttp://hdl.handle.net/2440/24002
dc.language.isoen
dc.publisherBlackwell Science Ltd
dc.source.urihttps://doi.org/10.1111/j.1365-2605.2005.00574.x
dc.subjectTestis
dc.subjectLeydig Cells
dc.subjectSertoli Cells
dc.subjectAnimals
dc.subjectHumans
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectPrenatal Exposure Delayed Effects
dc.subjectDisease Models, Animal
dc.subjectDibutyl Phthalate
dc.subjectAndrogen Antagonists
dc.subjectMaternal Exposure
dc.subjectPregnancy
dc.subjectFemale
dc.subjectMale
dc.titleCellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate
dc.typeJournal article
pubs.publication-statusPublished

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