PROGESTERONE RECEPTOR SIGNALING IS IMPAIRED IN THE PUBERTAL MAMMARY GLAND AFTER THE INTRAUTERINE EXPOSURE TO THE UV-FILTER BENZOPHENONE-3

SCHIERANO-MAROTTI GONZALO; ALTAMIRANO GABRIELA ANAHI; GOMEZ AYELEN LUCIANA; SOFIA LORENA ODDI; MUÑOZ-DE-TORO MÓNICA; KASS LAURA

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias; 2022

Sociedad de Biociencias

Mammary gland development is sensitive to endocrine disruption by environmental contaminants like the UV-filter benzophenone-3 (BP3), widely utilized in personal care products. Our aim was to evaluate whether intrauterine exposure to BP3 affects the progesterone receptor (RP) signaling in he mammary gland during puberty. Pregnant C57BL/6 mice were dermally exposed to vehicle sesame oil; Control), 0.15 (0.15-BP3) or 50mg BP3/kg/day (50-BP3) from gestation day 8.5 to 18. Serum and mammary gland samples were taken from the female offspring on postnatal day 45 ± 3 at diestrus 1. Serum levels of estradiol (E2) and progesterone (P4) were assessed. In the mammary gland, the histoarchitecture and quantification of mast cells were performed in histological sections stained with hematoxylin-eosin and alcian-blue/safranin, respectively. The mRNA expression of estrogen receptor alpha (ESR1), PR, RANKL and WNT4 (both PR-induced genes) was assessed by real-time RT-PCR. Serum levels of E2 and P4, the histoarquitecture, and the number of mast cells were similar between all experimental groups (p > 0.05). The expression level of PR was below the limit of quantification in 3 of 6 and 4 of 7 animals in the 0.15-BP3 and 50-BP3 groups, respectively. Similarly, in those animals, WNT4 expression was also negligible. In contrast, RANKL and ESR1 expression of BP3-exposed groups was similar between groups (p > 0.05). Our results showed that intrauterine BP3-exposure could impair the PR signaling pathway, and therefore, affect the normal development of the mouse mammary gland during puberty