Molecular Dynamics and Quantum Chemical Insights into the Molecular Basis of Differential Toxicity of the Mycotoxin Deoxynivalenol (DON) and Its Microbial Derivatives DOM‑1 and 3-epi-DON

利用分子动力学和量子化学方法揭示霉菌毒素脱氧雪腐镰刀菌烯醇 (DON) 及其微生物衍生物 DOM-1 和 3-epi-DON 毒性差异的分子基础

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Abstract

Deoxynivalenol (DON) is a trichothecene mycotoxin from Fusarium species that contaminates cereal grains, posing health risks. DON binds to site A of the 60S ribosomal subunit in eukaryotes, triggering a ribotoxic stress response. Despite structural similarity, its metabolites, deepoxy-deoxynivalenol (DOM-1) and 3-epi-deoxynivalenol (3-epi-DON), are nontoxic, but the molecular basis of this difference is unclear. This study employed molecular docking, molecular dynamics (MD) simulations, and quantum chemical calculations based on Symmetry-Adapted Perturbation Theory (SAPT) to analyze the interactions of DON and its metabolites with the ribosomal site. Our results reveal that DON adopts a unique binding conformation, enabling strong and stable interactions with an Mg(2+) ion and nucleotide U2873, maintaining its position within the ribosomal pocket throughout 500 ns of MD simulations. In contrast, DOM-1 and 3-epi-DON fail to sustain these interactions due to the absence of the epoxide group or altered hydroxyl orientation, leading to their dissociation. Additional MD simulations of the complex with another potent toxic trichothecene, verrucarin A showed stable binding at the same site, emphasizing the importance of these molecular interactions for toxicity. Further, quantum chemical analyses highlighted the energetic contributions of electrostatic and induction forces in stabilizing DON within the binding pocket. These data are in line with experimental studies in HCT116 human colon cancer cells confirming the lack of cytotoxicity of DOM-1 and 3-epi-DON and demonstrating differential ribotoxicity of DON and its metabolites. These results highlight a clear structure-activity relationship, where modifications at key positions markedly affect trichothecene binding and toxicity. Together, these findings advance our understanding of trichothecene toxicity and support the development of detoxification strategies and novel therapeutics targeting this ribosomal site.

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