SAT-138 - Environmental Insults in Rats Induce Central Precocious Puberty

We previously reported that perinatal exposure to dioxins, a class of persistent organic pollutants, induces precocious puberty-like phenotypes in female rats, effects most consistent with central precocious puberty, indicating that environmental insults are possible to affect female reproductive health. In the present study, to determine whether the postnatal social environment during development influences pubertal development, sexual maturation in female Long-Evans rats subjected to early weaning was examined. Female pups were weaned on postnatal day (PND) 15, and the timing of vaginal opening and first estrus was recorded. In early-weaned animals, vaginal opening and first estrus occurred approximately 4-7 days earlier than in vehicle-exposed control offspring. Early weaning also accelerated ovarian weight gain. We further assessed ovarian compensatory hypertrophy (OCH) as an index of maturation of the hypothalamic-pituitary gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) axis. For OCH assessment, a predetermined number of animals in each group underwent hemi-ovariectomy under light diethyl ether anesthesia on PND 15, 20, 25, 30, 35, or 40. The remaining ovary was collected 7-10 days post-surgery, on the morning estrus was confirmed by vaginal cytology. Histological analyses were performed on ovaries obtained from hemi-ovariectomized animals at each developmental stage. Early weaning advanced the onset of OCH. Specifically, compensatory hypertrophy-characterized by hyper-ovulation and a marked increase in the mass of the remaining ovary following hemi-ovariectomy was observed on PND 27-30, approximately 10 days earlier than in the control group weaned on PND 28. Collectively, these findings indicate that early weaning induces precocious puberty in female rats, including accelerated maturation of the hypothalamic-pituitary axis as well as the gonads and external genitalia. The maturation of the hypothalamus, ovary and pituitary are prerequisites for the onset of OCH, indicating that the negative feedback of estrogen and the GnRH-surge secretion cooperatively functions. Thus, the onset of OCH can be an excellent index for the maturation of the hypothalamus. These data further suggest the need for additional studies to elucidate the relationships between environmental factors and endocrine disorders in females, including precocious puberty.

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