ESPE Abstracts

Background: It is now widely accepted that chemical pollutants in the environment can interfere with the endocrine system. The impact of endocrine disrupting chemicals on puberty disorders is concerned. bisphenol-A (BPA) has been measured in fetal plasma. There are different toxic effects with different doses of BPA.

Objective and hypotheses: To observe vaginal opening day (VOD) hypothalamic kiss-1 gene and ovarian estrogen receptors (ER) gene expression level changes in neonatal rats exposure to different doses of BPA.

Method: Neonatal female SD rats were randomly divided into six groups: control group, vehicle group, 17β-estradiol group (17β-estradiol (E₂), 10 μg/day), low-dose BPA group (25 μg/kg per day), medium-dose BPA group (50 μg/kg per day), and high-dose BPA group (250 μg/kg per day). The rats got seven s.c. injections over postnatal day (PND) 0–6 and were sacrificed on the VOD and weighed. The VOD was recorded. The hypothalamus and ovaries were removed, weighed and calculated the organ/body weight ratio. Real-time PCR were used to observe the mRNA level changes of hypothalamic kiss-1 gene and ovarian ER gene.

Results: Data suggests that neonatal 50 and 250 μg/kg per day BPA exposure induced premature puberty of rat, but it may not result from the expression level changes of hypothalamic kiss-1 mRNA; neonatal 25 μg/kg per day BPA exposure did not induce premature puberty of rat.

Conclusion: Neonatal 50 and 250 μg/kg per day BPA exposure induced premature puberty of rat. The premature puberty above mentioned was not caused by the changes of the hypothalamic kiss-1 mRNA and its protein expression. Neonatal 25 μg/kg per day BPA exposure did not induce premature puberty of rat.