Prenatal Exposure to Bisphenol A and Diethylhexyl Phthalate Induces Hyperprolactinemia in Female offspring

Exposure to endocrine disrupting chemicals (EDC) such as Bisphenol A (BPA) and Diethylhexyl Phthalate (DEHP) are widespread affecting people of all ages. Pregnant women who are exposed to these chemicals through the use of personal care products and plastics invariably expose their fetus to these chemicals as well. Female offspring are then exposed to endogenous estrogens from menarche till menopause and usually, in their prime years, they are also exposed to estrogens through oral contraceptives. This places them at increased risk of developing hyperprolactinemia which causes infertility. In order to mimic real‐life exposures, we developed the “dual exposure paradigm” where we administered saline, 5μg/Kg BW of BPA, 7.5mg/kg BW of DEHP or a combination of BPA+DEHP to pregnant Sprague Dawley rats from day 6–21 of gestation. Female offspring were sham implanted or implanted with slow release estradiol‐17β (E2) pellets for 90 days when they were 3 months old. At the end of E2 treatment, animals were sacrificed, and the brain was removed, frozen and sectioned. We hypothesized that the dual exposure to EDCs and E2 would decrease dopamine (DA) levels in the median eminence of the hypothalamus to increase prolactin levels. The median eminence was microdissected from the brains and DA levels were measured using HPLC‐EC. Serum prolactin levels were assessed by EIA. DA levels in E2‐treated control rats were significantly reduced compared to sham‐implanted rats (p<0.001). Prenatal exposure to EDCs produced a modest reduction in DA levels in sham implanted rats (p<0.05) but decreased further with E2 treatment (p<0.001). Prolactin levels in control animals were significantly higher in E2 implanted rats compared to sham(p<0.05). Prolactin levels in EDC‐exposed rats were variable and were higher than normal in both sham and E2 treated animals. These results indicate that dual exposure to EDC and E2 is able to affect TIDA activity and induce hyperprolactinemia in female offspring. This could have implications in the development of mammary and pituitary tumors. Support or Funding Information Supported by UGA research foundation and startup funds. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .