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Excess androgen during perinatal life alters steroid receptor expression, apoptosis, and cell proliferation in the uteri of the offspring
  • Universidade Estadual de Campinas (UNICAMP)
  • Universidade Estadual Paulista (UNESP)
  • University of North Carolina
  • 0890-6238
  • 1873-1708
Exposure 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.
Issue Date: 
Reproductive Toxicology, v. 40, p. 1-7.
Time Duration: 
  • Female reproduction
  • Hyper-androgenic condition
  • Immunohistochemistry
  • Steroid receptors
  • Uterus
  • androgen
  • androgen receptor
  • cycline
  • estrogen receptor alpha
  • progesterone receptor
  • steroid receptor
  • testosterone propionate
  • animal cell
  • animal experiment
  • animal tissue
  • apoptosis
  • cell proliferation
  • controlled study
  • female
  • immunohistochemistry
  • lactation
  • nonhuman
  • perinatal drug exposure
  • rat
  • uterus
  • uterus weight
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Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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