Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, Shanxi 030001, China.
Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, Shanxi 030001, China.
Chemosphere. 2020 Sep;254:126608. doi: 10.1016/j.chemosphere.2020.126608. Epub 2020 Mar 29.
AlO Nanoparticles (AlO-NPs) have been widely used because of their unique physical and chemical properties, and AlO-NPs can be released into the environment directly or indirectly. Our previous research found that 13 nm AlO-NPs can induce neural cell death and autophagy in primarily cultured neural cells in vitro. The aim of this study was to determine where AlO-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 AlO-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 AlO-NPs significantly declined, and the ultramicroscopic morphology indicated profound autophagy alternations. The results suggest that AlO-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 AlO-NPs on learning and memory during the development of zebrafish from embryo to adult.
氧化铝纳米颗粒（AlO-NPs）由于其独特的物理和化学性质而被广泛应用，并且 AlO-NPs 可以直接或间接地释放到环境中。我们之前的研究发现，13nm AlO-NPs 可以在体外诱导原代培养的神经细胞死亡和自噬。本研究旨在确定 13nm 粒径的 AlO-NPs 在体内何处能引起神经细胞损伤，并评估相关的行为变化及其潜在的机制。我们选择斑马鱼从胚胎到成年期作为动物模型。在从胚胎到成年期的发育过程中，测量斑马鱼的学习和记忆等神经细胞的功能指标。研究结果表明，AlO-NPs 处理斑马鱼胚胎阶段可导致斑马鱼脑组织中铝含量的积累，导致神经发育行为逐渐受损，潜在的学习和记忆表现受损。此外，斑马鱼脑组织中的氧化应激和多巴胺能传递的破坏与铝含量的剂量依赖性和年龄依赖性积累相关。此外，用 AlO-NPs 处理的端脑组织中的神经细胞数量明显减少，超微形态学显示自噬发生了深刻变化。研究结果表明，AlO-NPs 在胚胎期处理时，对成年斑马鱼的学习和记忆表现具有剂量依赖性和时间依赖性的渐进性损伤。这是首次研究 AlO-NPs 在斑马鱼从胚胎到成年发育过程中对学习和记忆的影响。
