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Progressive impairment of learning and memory in adult zebrafish treated by Al2O3 nanoparticles when in embryos.
Chemosphere ( IF 8.1 ) Pub Date : 2020-03-29 , DOI: 10.1016/j.chemosphere.2020.126608
Jin Chen 1 , Rong Fan 1 , Yanhong Wang 1 , Tao Huang 1 , Nan Shang 1 , Kaihong He 1 , Ping Zhang 1 , Ling Zhang 1 , Qiao Niu 1 , Qinli Zhang 1
Affiliation  

Al2O3 Nanoparticles (Al2O3-NPs) have been widely used because of their unique physical and chemical properties, and Al2O3-NPs can be released into the environment directly or indirectly. Our previous research found that 13 nm Al2O3-NPs can induce neural cell death and autophagy in primarily cultured neural cells in vitro. The aim of this study was to determine where Al2O3-NPs at 13 nm particle size can cause neural cells in vivo and assess related behavioural changes and involved potential mechanisms. Zebrafish from embryo to adult were selected as animal models. Learning and memory as functional indicators of neural cells in zebrafish were measured during the development from embryo to adult. Our results indicate that Al2O3-NPs treatment in zebrafish embryos stages can cause the accumulation of aluminium content in zebrafish brain tissue, leading to progressive impaired neurodevelopmental behaviours and latent learning and memory performance. Additionally, oxidative stress and disruption of dopaminergic transmission in zebrafish brain tissues are correlated with the dose-dependent and age-dependent accumulation of aluminium content. Moreover, the number of neural cells in the telencephalon tissue treated with Al2O3-NPs significantly declined, and the ultramicroscopic morphology indicated profound autophagy alternations. The results suggest that Al2O3-NPs has dose-dependent and time-dependent progressive damage on learning and memory performance in adult zebrafish when treated in embryos. This is the first study of the effects of Al2O3-NPs on learning and memory during the development of zebrafish from embryo to adult.



中文翻译:

Al2O3纳米粒子处理成年斑马鱼在胚胎中的学习和记忆进行性损害。

Al 2 O 3纳米颗粒(Al 2 O 3 -NPs)由于其独特的物理和化学性质而被广泛使用,并且Al 2 O 3 -NPs可以直接或间接释放到环境中。我们以前的研究发现13 nm Al 2 O 3 -NPs可以在体外培养的主要神经细胞中诱导神经细胞死亡和自噬。这项研究的目的是确定Al 2 O 3在哪里13 nm粒径的-NPs可以在体内引起神经细胞并评估相关的行为变化和涉及的潜在机制。选择从胚胎到成年的斑马鱼作为动物模型。在从胚胎到成年的发育过程中,学习和记忆是斑马鱼神经细胞功能的指标。我们的结果表明Al 2 O 3斑马鱼胚胎阶段中的-NPs治疗可导致斑马鱼脑组织中铝含量的积累,从而导致神经发育行为的进行性受损以及潜在的学习和记忆能力下降。另外,斑马鱼脑组织中的氧化应激和多巴胺能传递的中断与铝含量的剂量依赖性和年龄依赖性积累有关。此外,用Al 2 O 3 -NPs处理的末梢脑组织中的神经细胞数量显着减少,并且超显微形态表明自噬发生了深刻的交替。结果表明,Al 2 O 3当在胚胎中处理时,NPs对成年斑马鱼的学习和记忆性能具有剂量依赖性和时间依赖性的进行性损害。这是关于斑马鱼从胚胎到成年发育过程中Al 2 O 3 -NPs对学习和记忆的影响的首次研究。

更新日期:2020-03-30
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