Progressive impairment of learning and memory in adult zebrafish treated by Al2O3 nanoparticles when in embryos. (September 2020)

• Record Type: Journal Article
• Authors: Chen, Jin; Fan, Rong; Wang, Yanhong; Huang, Tao; Shang, Nan; He, Kaihong; Zhang, Ping; Zhang, Ling; Niu, Qiao; Zhang, Qinli
• Is Part Of: Chemosphere. Volume 254(2020)
• Publication Date: 2020-09
• Subjects: Al2O3 nanoparticles -- Zebrafish -- Learning and memory -- Neuroethology -- Oxidative stress -- Neurotransmitters; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2020.126608
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: Al2 O3 Nanoparticles (Al2 O3 -NPs) have been widely used because of their unique physical and chemical properties, and Al2 O3 -NPs can be released into the environment directly or indirectly. Our previous research found that 13 nm Al2 O3 -NPs can induce neural cell death and autophagy in primarily cultured neural cells in vitro. The aim of this study was to determine where Al2 O3 -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 Al2 O3 -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 Al2 O3 -NPs significantly declined, and the ultramicroscopic morphology indicated profound autophagy alternations. The results suggest that Al2 O3 -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 Al2 O3 -NPs on learning and memory during the development of zebrafish from embryo to adult. Graphical abstract: Image 1 Highlights: Al2 O3 -NPs causes progressive impairment of learning and memory during the development of zebrafish from embryo to adult. Impairment of zebrafish embryos induced by Al2 O3 -NPs can last and aggregate until they grow up to become adults. Neural cell death and autophagy may be involved in the mechanism of progressive learning and memory deficits. Al2 O3 -NPs can cause oxidative stress in the brain of adult zebrafish after exposure to Al2 O3 -NPs in its embryo stage.