title: Temporal window in which exposure to estradiol permanently modifies ovarian function causing polycystic ovary morphology in rats.
abstract: OBJECTIVE
  To investigate the developmental window in which E(2) exposure produces irreversible changes in ovarian function resulting in polycystic ovary.
  
  
  METHODS
  Basic experimental study.
  
  
  METHODS
  University animal laboratory.
  
  
  METHODS
  Thirty Sprague-Dawley rats were administered a single E(2) valerate dose (10 mg/kg of weight) at 1, 7, 14, 21, or 30 days of age. Control rats were injected with the vehicle at 1 day of age. All rats were sacrificed at 6 months of age.
  
  
  METHODS
  Observation of vaginal opening, estrous cyclicity by vaginal smears, and ovarian morphometry in the 6-month-old rat.
  
  
  METHODS
  Measurement of ovarian noradrenaline by high-performance liquid chromatography coupled with electrochemical detection, serum levels of LH by enzyme-linked immunoassay, P, androstenedione, and E(2) by enzyme immunoassay.
  
  
  RESULTS
  Rats exposed to E(2) at 1, 7, or 14 days of life did not show estrual cycling activity and maintained a polycystic ovary (PCO) condition throughout the entirety of the study. However, if the exposure to E(2) occurred after postnatal day 21, the PCO-induced condition was reversible. In rats that developed a permanent PCO condition, we observed significant effects of E(2) on ovarian morphology if exposure occurred on postnatal day 1 and a presumable effect on the hypothalamus if the exposure occurred between postnatal days 1 and 14.
  
  
  CONCLUSIONS
  Our findings suggest that in rats, the most sensitive period for the promotion of an irreversible PCO morphology by estrogenic compounds is during neonatal early follicular development.
authors.affiliation: Laboratory of Neurobiochemistry, Faculty of Chemistry and Pharmaceutical Sciences, Universidad de Chile, Santiago, Chile.
authors.forename: Gonzalo
authors.initials: G
authors.lastname: Cruz
authors.forename: Rafael
authors.initials: R
authors.lastname: Barra
authors.forename: Daniel
authors.initials: D
authors.lastname: González
authors.forename: Ramón
authors.initials: R
authors.lastname: Sotomayor-Zárate
authors.forename: Hernán E
authors.initials: HE
authors.lastname: Lara
mesh_terms: D000367:Age Factors; D000735:Androstenedione / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D015415:Biomarkers / Q000097:blood; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D055664:Electrochemical Techniques; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000031:analogs & derivatives*; D030762:Estrous Cycle; D005260:Female; D007986:Luteinizing Hormone / Q000097:blood; D009638:Norepinephrine / Q000378:metabolism; D006080:Ovarian Follicle / Q000378:metabolism / Q000473:pathology; D010053:Ovary / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D010060:Ovulation; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D011374:Progesterone / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014621:Vagina / Q000254:growth & development / Q000378:metabolism / Q000473:pathology
chemical_list: D015415:Biomarkers; D000735:Androstenedione; D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D009638:Norepinephrine