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首页> 外文期刊>CNS neuroscience & therapeutics. >β‐Phenethylamine—A Phenylalanine Derivative in Brain—Contributes to Oxidative Stress by Inhibiting Mitochondrial Complexes and DT ‐Diaphorase: An iIn Silico/i Study
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β‐Phenethylamine—A Phenylalanine Derivative in Brain—Contributes to Oxidative Stress by Inhibiting Mitochondrial Complexes and DT ‐Diaphorase: An iIn Silico/i Study

机译：β-苯乙胺（一种大脑中的苯丙氨酸衍生物）通过抑制线粒体复合物和DT心肌酶来促进氧化应激：计算机模拟研究

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Summary Aim Till date, the mode of action of β‐ PEA on neurons is not well illustrated. We tested the hypothesis that β– PEA has the ability to cause oxidative stress by inhibiting the antioxidant enzyme DT ‐diaphorase and mitochondrial complexes ( C omplex‐I and complex‐ III ). Methods Using molecular docking as a tool, we here studied and compared the inhibitory capacity of β‐ PEA on DT ‐diaphorase and mitochondrial complexes. Three‐dimensional structures of mitochondrial complexes and DT ‐diaphorase and their ligands were downloaded from the respective data banks, and free energy of binding (docking scores) were determined. Results The present finding demonstrated for the first time that β‐ PEA potentiates reactive oxygen species generation by inhibiting the antioxidant enzyme DT ‐diaphorase, in addition to the mitochondrial complex‐I and complex‐ III . Conclusion As lowering of cellular antioxidant molecules is evident in many neurodegenerative disorders, β‐ PEA ‐induced lowering of DT ‐diaphorase activity may have the capability to cause neurodegeneration, which may be potentiated by its ability to inhibit mitochondrial complexes. Thus, β‐ PEA —due to its cumulative actions—may be more potent in causing neurodegeneration as compared to other endogenous neurotoxins.
机译：总结迄今为止，尚未很好地阐明β-PEA对神经元的作用方式。我们检验了以下假设：β-PEA能够通过抑制抗氧化酶DT心肌黄递酶和线粒体复合物（复合体I和复合体III）而引起氧化应激。方法我们使用分子对接作为工具，研究并比较了β-PEA对DT心肌黄递酶和线粒体复合物的抑制能力。从各自的数据库中下载线粒体复合物和DT心肌黄递酶及其配体的三维结构，并确定了结合自由能（对接分数）。结果本发现首次证明，β-PEA除线粒体complex-I和complex-III外，还通过抑制抗氧化酶DT-diaphorase增强了活性氧的生成。结论由于许多神经退行性疾病中细胞抗氧化剂分子的降低很明显，因此β-PEA诱导的DT-心肌黄递酶活性的降低可能具有引起神经变性的能力，这可能是由于其抑制线粒体复合物的能力所致。因此，与其他内源性神经毒素相比，由于其累积作用，β-PEA可能更有效地引起神经变性。

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