Carcinogenesis, Teratogenesis & Mutagenesis ›› 2010, Vol. 22 ›› Issue (3): 196-201.doi: 10.3969/j.issn.1004-616x.2010.03.009

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The effect of perinatal exposure to Bisophenol A on reproductive system of female offspring rats and changes in expression of estrogen receptor

CHEN Yin-chang;HAO Wei-dong;SHANG Lan-qin;WEI Xue-tao;JIANG Jian-jun;LIU Ran;XING Li-na;WU Shuang   

  1. Department of Toxicology, School of Public Health, Peking University, Beijing 100191, China
  • Received:2010-03-05 Revised:2010-03-20 Online:2010-05-30 Published:2010-05-30
  • Contact: HAO Wei-dong

Abstract: OBJECTIVE: To explore the effect of perinatal exposure to bisophenol A(BPA) on reproduction and development of the female offspring of SD rats and the changes of uterine estrogen receptor(ER) expression. METHODS: Pregnant Sprague-Dawley rats received by gavage 0, 5, 50 or 500 mg/(kg•d) of BPA from gestation day (PND) 6 to postnatal day (PND) 21. Uterus and ovarians were weighed and prepared for histological evaluation. The expression of ERα, ERβ, phosphorylated ERK (p-ERK) and total ERK (T-ERK) in uterus were measured. The change of uterine sensitivity to estradiol (E2) was investigated by the modified uterotrophic assay. RESULTS: The toxic symptoms in parental rats and decrease in body weight in female offsprings were observed in 500 mg/(kg•BW) group, but there was an increase in body weight and uterine weight in the 50 mg/(kg•BW) group. No pathological changes were found in BPA- treated group, the thickness of endometrial layer and the ratio to uterus was increased in all dosage groups compared with the control. The protein expressions of ERα and p-ERK but not ERβ in uterus were elevated in all dosage groups. The uterine sensitivity to E2 was increased in all BPA-treated groups. CONCLUSION: Perinatal exposure to Bisphenol A could induce the changes of ER expression in the uterus of female offspring rats and change the uterine physical structure by probably activating the ERK pathway.

Key words: Bisphenol A, female offspring, reproductive and developmental effects, estrogen receptor, extracellular regulated kinase

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