The Role of Cholesterol in the Interaction of the Lipid Monolayer with the Endocrine Disruptor Bisphenol-A

Among pollutants of emerging concern, endocrine disruptors (ED) have been shown to cause side effects in humans and animals. Bisphenol-A (BPA) is an ED by-product of the plastic industry and one of the chemicals with the highest volume produced yearly. Here, we studied the role of cholesterol in the BPA exposure effects over membrane models. We used Langmuir films of both neat lipid DPPC (1,2-dipalmitoyl-sn-glycero-3-phosphocholine) and cholesterol (Chol) and a binary mixture containing DPPC/Chol, exposing it to BPA. We evaluate changes in the π-A isotherms and the PM–IRRAS (polarization modulation–infrared reflection adsorption spectroscopy) spectra. BPA exposure induced changes in the DPPC and Chol neat monolayers, causing mean molecular area expansion and altering profiles. However, at high surface pressure, the BPA was expelled from the air–water interface. For the DPPC/Chol mixture, BPA caused expansion throughout the whole compression, indicating that BPA is present at the monolayer interface. The PM–IRRAS analysis showed that BPA interacted with the phosphate group of DPPC through hydrogen bonding, which caused the area’s expansion. Such evidence might be biologically relevant to better understand the mechanism of action of BPA in cell membranes once phosphatidylcholines and Chol are found in mammalian membranes.