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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/76419
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dc.contributor.authorGuerra, Marina T.-
dc.contributor.authorSanabria, Marciana-
dc.contributor.authorGrossman, Gail-
dc.contributor.authorPetrusz, Peter-
dc.contributor.authorKempinas, Wilma de Grava-
dc.date.accessioned2014-05-27T11:30:32Z-
dc.date.accessioned2016-10-25T18:53:11Z-
dc.date.available2014-05-27T11:30:32Z-
dc.date.available2016-10-25T18:53:11Z-
dc.date.issued2013-09-01-
dc.identifierhttp://dx.doi.org/10.1016/j.reprotox.2013.05.001-
dc.identifier.citationReproductive Toxicology, v. 40, p. 1-7.-
dc.identifier.issn0890-6238-
dc.identifier.issn1873-1708-
dc.identifier.urihttp://hdl.handle.net/11449/76419-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/76419-
dc.description.abstractExposure to environmental chemicals may contribute to reproductive disorders, especially when it occurs in critical periods of development. The female reproductive system can be a target for androgens derived from environmental contaminants or pathological conditions. The purpose of this study was to assess the long-term effects of androgens on uterine tissue after maternal exposure limited to the time of gestation and lactation. Pregnant Wistar rats were treated with testosterone propionate (TP) at 0.05. mg/kg, 0.1. mg/kg, 0.2. mg/kg or corn oil (vehicle), s.c., from gestational day 12 until the end of lactation. The results show changes in the pattern of expression of receptors for estrogen, progesterone, and androgen at all doses tested, and decreases in both apoptosis and cell proliferation indices at 0.1 and 0.2. mg/kg. We conclude that early TP exposure, under these experimental conditions, causes changes in cellular and molecular parameters that are essential for normal uterine function in the adult. © 2013 Elsevier Inc.en
dc.format.extent1-7-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectFemale reproduction-
dc.subjectHyper-androgenic condition-
dc.subjectImmunohistochemistry-
dc.subjectSteroid receptors-
dc.subjectUterus-
dc.subjectandrogen-
dc.subjectandrogen receptor-
dc.subjectcycline-
dc.subjectestrogen receptor alpha-
dc.subjectprogesterone receptor-
dc.subjectsteroid receptor-
dc.subjecttestosterone propionate-
dc.subjectanimal cell-
dc.subjectanimal experiment-
dc.subjectanimal tissue-
dc.subjectapoptosis-
dc.subjectcell proliferation-
dc.subjectcontrolled study-
dc.subjectfemale-
dc.subjectimmunohistochemistry-
dc.subjectlactation-
dc.subjectnonhuman-
dc.subjectperinatal drug exposure-
dc.subjectrat-
dc.subjectuterus-
dc.subjectuterus weight-
dc.titleExcess androgen during perinatal life alters steroid receptor expression, apoptosis, and cell proliferation in the uteri of the offspringen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversity of North Carolina-
dc.description.affiliationGraduate Program in Cell and Structural Biology Institute of Biology State University of Campinas - UNICAMP, Campinas, SP-
dc.description.affiliationInstitute of Biosciences Universidade Estadual Paulista (UNESP) Department of Morphology, Botucatu, SP-
dc.description.affiliationDepartment of Cell and Developmental Biology Laboratories for Reproductive Biology University of North Carolina, Chapel Hill, NC-
dc.description.affiliationUnespInstitute of Biosciences Universidade Estadual Paulista (UNESP) Department of Morphology, Botucatu, SP-
dc.identifier.doi10.1016/j.reprotox.2013.05.001-
dc.identifier.wosWOS:000322849300001-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofReproductive Toxicology-
dc.identifier.scopus2-s2.0-84879518314-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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