Abstract: Alcohol functions as an endocrine disruptor, and has been shown to increase the risk of breast cancer. This risk may be augmented by involuntary exposure to environmental endocrine disrupting chemicals, such as phthalates. Phthalates are a group of endocrine disrupting chemicals used as plasticizers, and are found in a wide range of products including personal-care products, cosmetics and food packaging. Exposure to these compounds during development is associated with precocious puberty and early mammary gland development, risk factors for breast cancer (Golestanzadeh, Riahi and Kelishadi, 2020). Given the potential initiation of alcohol drinking during adolescence/puberty, a window of susceptibility for breast cancer, we first became interested in describing hormone mechanisms that may underlie alcohol’s effects on the developing mammary gland. Our preliminary experiment used C57BL/6J mice as an in vivo approach to explore the impact that voluntary binge drinking during puberty/adolescence may have on features of mammary development susceptible to hormone disruption, like branching and terminal end bud formation. Mice were given two weeks of limited access to ethanol where they binge drank daily (3.87 – 9.19 g/kg/3hrs). In order to explore the potential synergistic effects of phthalate and alcohol exposure on progesterone and estrogen signaling we next turned to a cell based model. Using the T47D breast cancer cell line, we explored whether exposure to phthalate (DEHP at 10nM or 10,000nM) alongside ethanol (25mM or 50mM) would impact progesterone and estrogen signaling in these cells. Cells were serum starved for three days and treated with Ethanol with or without DEHP for four days. Trizol was used to isolate RNA and protein from mammary glands of ethanol exposed mice and Ethanol/DEHP exposed TD47 cells. The in vivo data supported considerable changes in terminal end bud formation and marginal reductions in mammary gland branching following pubertal binge drinking in mice. Ongoing work is being conducted to compare the effects of ethanol and phthalate on progesterone and estrogen signaling in these samples.
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