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Acute Effects of Pulmonary Exposure to Zinc Oxide Nanoparticles on Brain in vivo

Category: Air Pollution and Health Effects

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DOI: 10.4209/aaqr.2019.10.0523
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To cite this article:
Chuang, H.C., Yang, Y.T., Chen, H.C., Hwang, Y.H., Wu, K.Y., Chen, T.F., Chen, C.L., Jhan, M.K. and Cheng, T.J. (2020). Acute Effects of Pulmonary Exposure to Zinc Oxide Nanoparticles on Brain in vivo. Aerosol Air Qual. Res., doi: 10.4209/aaqr.2019.10.0523.

Hsiao-Chi Chuang1,2,3, Yu-Ting Yang4, Hsin-Chang Chen5, Yaw-Huei Hwang4,6, Kuen-Yuh Wu4, Ta-Fu Chen7, Chia-Ling Chen1, Ming-Kai Jhan8,9, Tsun-Jen Cheng 4,5

  • 1 School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
  • 2 Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan
  • 3 Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei 23561, Taiwan
  • 4 Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei 10617, Taiwan
  • 5 Institute of Food Safety and Health, College of Public Health, National Taiwan University, Taipei 10617, Taiwan
  • 6 Department of Public Health, College of Public Health, National Taiwan University, Taipei 10617, Taiwan
  • 7 Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 10617, Taiwan
  • 8 Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
  • 9 Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan

Highlights

  • Neurotoxicity caused by PM was investigated.
  • Cytotoxicity and oxidative stress were occurred by PM.
  • PM-induced microglial activation.
  • Autophagy and apoptosis were regulated by PM.

Abstract

With applications of zinc oxide nanoparticles (ZnONP) continually increasing; however, the neurotoxicity of ZnONP remains unclear. The objective of the present study was to investigate the acute effects of pulmonary exposure to ZnONP on brain. We investigated the effects of ZnONP on behavioral alterations, oxidative stress, inflammation, and tau and autophagy expressions after acute pulmonary exposure. There were no significant alterations in spatial cognition or learning abilities according to the Morris water maze or anxiety according to the elevated-plus maze after ZnONP exposure. We observed that levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG)/dG were significantly increased in the hippocampus after exposure to 10 mg/kg ZnONP. We observed that levels of interleukin (IL)-1β and IL-6 significantly decreased in the cerebellum and cortex after exposure of 10 mg/kg ZnONP. Microglia activation occurred in the hippocampus after exposure. Significant tau expression was observed in the cerebellum and hippocampus with exposure to 10 mg/kg ZnONP, but no significant expressions of beclin 1, light chain 3 (LC3) II/I, or ubiquitin were observed. Results of the present study suggest that acute exposure of ZnONP induced oxidative stress, microglia activation and tau protein expression in brain, leading to neurotoxicity.

Keywords

Autophagy Central nervous system Elevated plus maze Morris water maze Nanoparticle Ubiquitin


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Accepted Manuscripts
DOI: 10.4209/aaqr.2019.12.0653
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