Bashirova Narmin, Schölzel Franziska, Hornig Dominik, Scheidt Holger A, Krueger Martin, Salvan Georgeta, Huster Daniel, Matysik Joerg, Alia A
Institute of Medical Physics and Biophysics, Leipzig University, D-04107 Leipzig, Germany.
Institute of Analytical Chemistry, Leipzig University, D-04103 Leipzig, Germany.
Molecules. 2025 Mar 24;30(7):1432. doi: 10.3390/molecules30071432.
Exposure of organisms to nanoplastics (NPs) is inevitable given their global abundance and environmental persistence. Polyethylene terephthalate (PET) is a common plastic used in a wide range of products, including clothing and food and beverage packaging. Recent studies suggest that NPs can cross the blood-brain barrier and cause potential neurotoxicity. It is widely known that aggregation of amyloid beta (Aβ) peptides in the brain is a pathological hallmark of Alzheimer's disease (AD). While the impact of nanoplastics such as polystyrene (PS) on amyloid aggregation has been studied, the effects of PET NPs remain unexplored. In this study, we examined the effect of PET NPs of different sizes (PET and PET) and concentrations (0, 10, 50, and 100 ppm) on the fibrillation of Aβ. Our results showed that the presence of PET as well as PET decreased the lag phase of the fibrillation processes in a dose- and size-dependent manner from 6.7 ± 0.08 h for Aβ in the absence of PET (Aβ) to 3.1 ± 0.03 h for PET and 3.8 ± 0.06 h for PET. CD spectroscopy showed that PET significantly impacts the structural composition of Aβ aggregates. A significant rise in antiparallel β-sheet content and β-turn structure and a substantial reduction in other structures were observed in the presence of 100 ppm PET. These changes indicate that higher concentrations (100 ppm) of PET promote more rigid and uniform peptide aggregates. Although PET NPs influence the kinetics of aggregation and secondary structure, the overall morphology of the resulting fibrils remains largely unaltered, as seen using transmission electron microscopy. Also, the local cross-β structure of the fibrils was not affected by the presence of PET NPs during fibrillation, as confirmed using C solid-state NMR spectroscopy. Overall, these findings show that PET NPs accelerate amyloid fibril formation and alter the secondary structure of Aβ fibrils. These results also indicate that the accumulation of PET-NPs in the brain may facilitate the progression of various neurodegenerative diseases, including Alzheimer's disease.
鉴于纳米塑料（NPs）在全球的广泛存在及其环境持久性，生物体不可避免地会接触到它们。聚对苯二甲酸乙二酯（PET）是一种常见的塑料，广泛用于各种产品，包括服装以及食品和饮料包装。最近的研究表明，纳米塑料可以穿过血脑屏障并导致潜在的神经毒性。众所周知，大脑中β-淀粉样蛋白（Aβ）肽的聚集是阿尔茨海默病（AD）的病理标志。虽然已经研究了聚苯乙烯（PS）等纳米塑料对淀粉样蛋白聚集的影响，但PET纳米塑料的影响仍未得到探索。在本研究中，我们研究了不同大小（PET和PET）和浓度（0、10、50和100 ppm）的PET纳米塑料对Aβ纤维化的影响。我们的结果表明，PET以及PET的存在以剂量和大小依赖的方式缩短了纤维化过程的延迟期，从无PET（Aβ）时Aβ的6.7±0.08小时分别缩短至PET的3.1±0.03小时和PET的3.8±0.06小时。圆二色光谱表明，PET显著影响Aβ聚集体的结构组成。在存在100 ppm PET的情况下，观察到反平行β-折叠含量和β-转角结构显著增加，而其他结构则大幅减少。这些变化表明，较高浓度（100 ppm）的PET促进了更刚性和均匀的肽聚集体的形成。尽管PET纳米塑料会影响聚集动力学和二级结构，但使用透射电子显微镜观察发现，所得纤维的整体形态在很大程度上保持不变。此外，使用13C固态核磁共振光谱证实，在纤维化过程中，纤维的局部交叉β结构不受PET纳米塑料存在的影响。总体而言，这些发现表明PET纳米塑料加速了淀粉样纤维的形成并改变了Aβ纤维的二级结构。这些结果还表明，PET纳米颗粒在大脑中的积累可能会促进包括阿尔茨海默病在内的各种神经退行性疾病的进展。
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