The Molecular Mechanism of Dicofol as an Agonist of the Human Estrogen Receptor: Insights from Molecular Docking and MM-GBSA Studies

The risk to human health has increased worldwide due to the widespread use of organochlorine pesticides. Dicofol (DCF), an organochlorine pesticide, is one of the most contentious endocrine disruptors; it can interact with nuclear receptors and interfere with their regular function. A member of the steroid hormone receptor family, the estrogen receptor (ER) is found in many bodily tissues. It binds to androgens and controls the activity of genes that are responsive to androgens. There is a chance that DCF will disrupt the estrogen receptor. In light of these specifics, we tested the ER disruption and related mechanisms of DCF using Molecular Docking, Generalized Born, and Surface Area Continuum Salvation (MM GBSA) in Molecular Mechanics. Dicofol may bind to the ER with efficiency, according to the docking results that were obtained. The MMGBSA results demonstrated that lipophilic interactions were the primary driver of the stable binding process. The current study supports the structural evidence that DCF is an endocrine disruptor and provides crucial guidance for finding safer alternatives.