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Zinc oxide nanoparticles effectively regulate autophagic cell death by activating autophagosome formation and interfering with their maturation.
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2020-09-18 , DOI: 10.1186/s12989-020-00379-7 Zixuan Liu 1 , Xuying Lv 1 , Lei Xu 1 , Xuting Liu 1 , Xiangyu Zhu 1 , Erqun Song 1 , Yang Song 1
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2020-09-18 , DOI: 10.1186/s12989-020-00379-7 Zixuan Liu 1 , Xuying Lv 1 , Lei Xu 1 , Xuting Liu 1 , Xiangyu Zhu 1 , Erqun Song 1 , Yang Song 1
Affiliation
With the development of zinc oxide nanoparticles (ZnO NPs) in the field of nanotechnology, their toxicological effects are attracting increasing attention, and the mechanisms for ZnO NPs neurotoxicity remain obscure. In an attempt to address concerns regarding neurotoxicity of ZnO NPs, we explored the relationship between free zinc ions, reactive oxygen species (ROS) and neurotoxic mechanisms in ZnO NPs-exposed PC12 cells. This study demonstrated the requirement of free zinc ions shed by ZnO NPs to over generation of intracellular ROS. Next, we identified autophagic cell death was the major mode of cell death induced by ZnO NPs, and autophagosome accumulation resulted from not only induction of autophagy, but also blockade of autophagy flux. We concluded that autophagic cell death, resulting from zinc ions-ROS-c-Jun N-terminal kinase (JNK)-autophagy positive feedback loop and blockade of autophagosomal-lysosomal fusion, played a major role in the neurotoxicity of ZnO NPs. Our study contributes to a better understanding of the neurotoxicity of ZnO NPs and might be useful for designing and developing new biosafety nanoparticles in the future.
中文翻译:
氧化锌纳米粒子通过激活自噬小体形成并干扰其成熟来有效调节自噬细胞的死亡。
随着纳米技术领域中氧化锌纳米颗粒(ZnO NPs)的发展,其毒理学作用日益引起人们的关注,而ZnO NPs神经毒性的机制仍不清楚。为了解决有关ZnO NPs神经毒性的问题,我们探索了暴露于ZnO NPs的PC12细胞中游离锌离子,活性氧(ROS)与神经毒性机制之间的关系。这项研究证明了ZnO NPs释放的游离锌离子对细胞内ROS过度生成的要求。接下来,我们确定自噬细胞死亡是ZnO NPs诱导细胞死亡的主要方式,并且自噬小体的积累不仅是由于自噬的诱导,而且是对自噬通量的阻断。我们得出结论,自噬细胞死亡,锌离子-ROS-c-Jun N末端激酶(JNK)-自噬正反馈回路和自噬体-溶酶体融合的阻滞,在ZnO NPs的神经毒性中起主要作用。我们的研究有助于更好地理解ZnO NPs的神经毒性,并可能在将来设计和开发新的生物安全纳米颗粒时有用。
更新日期:2020-09-20
中文翻译:
氧化锌纳米粒子通过激活自噬小体形成并干扰其成熟来有效调节自噬细胞的死亡。
随着纳米技术领域中氧化锌纳米颗粒(ZnO NPs)的发展,其毒理学作用日益引起人们的关注,而ZnO NPs神经毒性的机制仍不清楚。为了解决有关ZnO NPs神经毒性的问题,我们探索了暴露于ZnO NPs的PC12细胞中游离锌离子,活性氧(ROS)与神经毒性机制之间的关系。这项研究证明了ZnO NPs释放的游离锌离子对细胞内ROS过度生成的要求。接下来,我们确定自噬细胞死亡是ZnO NPs诱导细胞死亡的主要方式,并且自噬小体的积累不仅是由于自噬的诱导,而且是对自噬通量的阻断。我们得出结论,自噬细胞死亡,锌离子-ROS-c-Jun N末端激酶(JNK)-自噬正反馈回路和自噬体-溶酶体融合的阻滞,在ZnO NPs的神经毒性中起主要作用。我们的研究有助于更好地理解ZnO NPs的神经毒性,并可能在将来设计和开发新的生物安全纳米颗粒时有用。