Excess androgen during perinatal life alters steroid receptor expression, apoptosis, and cell proliferation in the uteri of the offspring

• Published in: Reproductive toxicology (Elmsford, N.Y.) Vol. 40; pp. 1 - 7
• Main Authors: Guerra, Marina T., Sanabria, Marciana, Grossman, Gail, Petrusz, Peter, Kempinas, Wilma de Grava
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-09-2013
• Subjects: Androgens - toxicity; Animals; Apoptosis - drug effects; Cell Proliferation - drug effects; Female; Female reproduction; Hyper-androgenic condition; Immunohistochemistry; Maternal-Fetal Exchange; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Wistar; Receptors, Steroid - metabolism; Steroid receptors; Testosterone Propionate - toxicity; Uterus; Uterus - cytology; Uterus - drug effects; Uterus - metabolism; Immunohistochemistry; Female reproduction; Uterus; Hyper-androgenic condition; Steroid receptors
• ISSN: 0890-6238; 1873-1708
• DOI: 10.1016/j.reprotox.2013.05.001

•Low-dose, prolonged exposure, as might occur with environmental contaminants.•Contributes to the understanding of reduced estrogen responsiveness of the uterus from androgenized rats.•Correlates androgen excess and progesterone and androgen receptors in the uterus.•Evaluates the dynamics of uterine growth/regression after androgen exposure.
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 0.05mg/kg, 0.1mg/kg, 0.2mg/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 0.2mg/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.