4.7 Article

Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice

Journal

CHEMOSPHERE
Volume 92, Issue 9, Pages 1183-1189

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2013.01.094

Keywords

Titanium dioxide nanoparticles; Brain; Reactive oxygen species; Macromolecule oxidation; Nrf-2 activation

Funding

  1. National Natural Science Foundation of China [81273036, 30901218]
  2. Priority Academic Program Development of Jiangsu Higher Education Institutions
  3. National Bringing New Ideas Foundation of Student of Soochow University [201210285036]

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Numerous studies have demonstrated that the brain is one of the target organs in acute or chronic titanium dioxide (TiO2) nanoparticles (NPs) toxicity, and oxidative stress plays an important role in this process. However, whether brain oxidative injury responds to TiO2 NPs by activating the P38-nuclear factor-E2-related factor-2 (Nrf-2) pathway is not fully understood. The present study aimed to examine activation of the P38-Nrf-2 signaling pathway associated with oxidative stress in the mouse brain induced by intranasal administration of TiO2 NPs for 90 consecutive days. Our findings indicate that TiO2 NPs caused overproliferation of spongiocytes and hemorrhage in the mouse brain. Furthermore, TiO2 NPs significantly activated p38, c-Jun N-terminal kinase, nuclear factor kappa B, Nrf-2 and heme oxygenase-1 expression in the brain, which in turn, led to increased production of reactive oxygen species, as well as lipid, protein and DNA peroxidation. These findings suggest that TiO2 NPs-induced oxidative damage in the mouse brain may occur via the p38-Nrf-2 signaling pathway. Therefore, application of TiO2 NPs in the environment should be performed with caution. Crown Copyright (C) 2013 Published by Elsevier Ltd. All rights reserved.

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