dc.contributorUniversidade Estadual de Campinas (UNICAMP)
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.contributorUniversity of North Carolina
dc.date.accessioned2014-05-27T11:30:32Z
dc.date.available2014-05-27T11:30:32Z
dc.date.created2014-05-27T11:30:32Z
dc.date.issued2013-09-01
dc.identifierReproductive Toxicology, v. 40, p. 1-7.
dc.identifier0890-6238
dc.identifier1873-1708
dc.identifierhttp://hdl.handle.net/11449/76419
dc.identifier10.1016/j.reprotox.2013.05.001
dc.identifierWOS:000322849300001
dc.identifier2-s2.0-84879518314
dc.identifier6326450271169741
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.
dc.languageeng
dc.relationReproductive Toxicology
dc.relation2.580
dc.relation0,846
dc.rightsAcesso restrito
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 offspring
dc.typeArtículos de revistas


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