Computational simulation study reveals that bisphenol analogues alter estrogen receptor-α allosteric dynamics, indicating alternative mechanisms beyond direct estrogen mimicry.
Bisphenol A (BPA) and related chemicals are widely present in the environment and can interact with hormone receptors in the body. The estrogen receptor alpha (ERα) is considered a key target of these endocrine-disrupting compounds. In this study, molecular docking, molecular dynamics simulations, and MM-PBSA calculations were used to evaluate the binding of twenty BPA derivatives to ERα. The docking method was first validated by re-docking and then compared using 17β-estradiol as a reference ligand. Among the tested compounds, Bisphenol PH (BPPH) showed the strongest docking score (− 11.4 kcal/mol), higher than 17β-estradiol (− 9.9 kcal/mol). Interaction analysis indicated that BPA and its analogues bind in the same estrogen pocket, mainly through hydrophobic interactions with few hydrogen bonds. At first, fifty-nanosecond MD simulations showed that the top-ranked complexes were structurally stable, with low RMSD changes, stable hydrogen bonding, and consistent pocket occupancy. The MM-PBSA analysis confirmed that BPPH has a favorable binding free energy with the receptor. A further extended MD simulation study (100 ns) showed the stability of the estrogen receptor-BPPH complex. Further, comparative dynamics cross-correlation matrix (DCCM) analysis showed that the BPPH modifies the native allosteric coupling between helix-12 and the core binding pocket relative to β-estradiol. This study shows that bisphenol analogs can change how ERα communicates with other proteins in different ways, instead of just acting like estrogens.
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Raghunath Satpathy (2026) studied this question.
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