Hormonal regulation controls mammary gland (MG) development. Therefore some hormone-related
factors can disrupt the early phases of MGs development, making the gland more susceptible
to long term modifications in its response to circulating hormones. Endocrine disruptors,
such as bisphenol A (BPA), are able to cause alterations in hormone receptor expression,
leading to changes in the cell proliferation index, which may expose the tissue to
neoplastic alterations. Thus, we evaluated the variations in hormone receptor expression
in the MG of 6-month old Mongolian gerbils exposed to BPA and 17 beta estradiol during
the perinatal period. Receptors for estrogen alpha (ER alpha), beta (ER beta), progesterone
(PGR), prolactin (PRL-R), and co-localization of connexin 43 (Cx43) and ER alpha in
gerbils were analyzed, and serum concentrations of estradiol and progesterone were
assessed. No alterations in body, liver, and ovary-uterus complex weights were observed.
However, there was an increase in epithelial ER alpha expression in the 17 beta estradiol
(E2) group and in PGR in the BPA group. Although immunohistochemistry did not show
alterations in ER beta expression, western blotting revealed a decrease in this protein
in the BPA group. PRL-R was more present in epithelial cells in the vehicle control
(VC), E2, and BPA groups in comparison to the intact control group. Cx43 was more
frequent in E2 and BPA groups, suggesting a protective response from the gland against
possible malignancy. Serum concentration of estradiol reduced in VC, E2, and BPA groups,
confirming that alterations also impacts steroid levels. Consequently, perinatal exposure
to BPA and the reference endogenous estrogen, 17 beta estradiol, are able to increase
the tendency of endocrine disruption in MG in a long term manner, since repercussions
are observed even 6 months after exposure.
