Chemistry Department, Faculty of Science, Beni-Suef University, Beni-Suef 62514, Egypt.
Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.
Molecules. 2024 Mar 22;29(7):1433. doi: 10.3390/molecules29071433.
This study provides a comprehensive computational exploration of the inhibitory activity and metabolic pathways of 8-methoxypsoralen (8-MP), a furocoumarin derivative used for treating various skin disorders, on cytochrome P450 (P450). Employing quantum chemical DFT calculations, molecular docking, and molecular dynamics (MD) simulations analyses, the biotransformation mechanisms and the active site binding profile of 8-MP in CYP1B1 were investigated. Three plausible inactivation mechanisms were minutely scrutinized. Further analysis explored the formation of reactive metabolites in subsequent P450 metabolic processes, including covalent adduct formation through nucleophilic addition to the epoxide, 8-MP epoxide hydrolysis, and non-CYP-catalyzed epoxide ring opening. Special attention was paid to the catalytic effect of residue Phe268 on the mechanism-based inactivation (MBI) of P450 by 8-MP. Energetic profiles and facilitating conditions revealed a slight preference for the C4'=C5' epoxidation pathway, while recognizing a potential kinetic competition with the 8-OMe demethylation pathway due to comparable energy demands. The formation of covalent adducts via nucleophilic addition, particularly by phenylalanine, and the generation of potentially harmful reactive metabolites through autocatalyzed ring cleavage are likely to contribute significantly to P450 metabolism of 8-MP. Our findings highlight the key role of Phe268 in retaining 8-MP within the active site of CYP1B1, thereby facilitating initial oxygen addition transition states. This research offers crucial molecular-level insights that may guide the early stages of drug discovery and risk assessment related to the use of 8-MP.
本研究通过量子化学 DFT 计算、分子对接和分子动力学(MD)模拟分析,对呋喃香豆素衍生物 8-甲氧基补骨脂素(8-MP)抑制细胞色素 P450(P450)的抑制活性和代谢途径进行了全面的计算探索。研究了 8-MP 在 CYP1B1 中的生物转化机制和活性部位结合模式,详细研究了三种可能的失活机制。进一步的分析探讨了在随后的 P450 代谢过程中形成的反应性代谢物,包括通过亲核加成到环氧化物形成共价加合物、8-MP 环氧化物水解和非 CYP 催化的环氧化物开环。特别关注了残基 Phe268 对 8-MP 引起的基于机制的失活(MBI)的催化作用。能量曲线和促进条件表明,C4'=C5'环氧化途径略有优势,而由于能量需求相当,8-OMe 去甲基化途径可能存在潜在的动力学竞争。亲核加成形成共价加合物,特别是由苯丙氨酸形成,以及通过自动催化环裂解产生潜在有害的反应性代谢物,可能对 8-MP 的 P450 代谢有重要贡献。我们的研究结果强调了 Phe268 在将 8-MP 保留在 CYP1B1 的活性部位中的关键作用,从而促进了初始氧添加过渡态的形成。这项研究提供了关键的分子水平见解,可能指导与使用 8-MP 相关的药物发现和风险评估的早期阶段。