alexa Nanosized TiO2 Exposure Resulted in Neurotoxicity via Impairing NMDA Receptor-mediated Postsynaptic Signaling Cascade in Mice | OMICS International | Abstract
ISSN: 2157-7439

Journal of Nanomedicine & Nanotechnology
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Research Article

Nanosized TiO2 Exposure Resulted in Neurotoxicity via Impairing NMDA Receptor-mediated Postsynaptic Signaling Cascade in Mice

Lei Sheng1#, Ling Wang2#, Yuguan Ze1#, Xiaoyang Zhao1#, Xiaohong Yu1, Jie Hong1, Dong Liu1, Bingqing Xu1, Xiaoyu Pan1, Anan Lin1, Yue Zhao1, Chi Zhang1, Yunting Zhu1, Yi Long1 and Fashui Hong1*

1Medical College of Soochow University, Suzhou 215123, China

2Library of Soochow University, Suzhou 215021, China

#equally to this work

*Corresponding Author:
Fashui Hong
Medical College of Soochow University
Suzhou 215123, China
Tel: +86-0512-61117563
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E-mail: [email protected]

Received Date: May 12, 2014; Accepted Date: June 02, 2014; Published Date: June 07, 2014

Citation: Sheng L, Wang L, Ze Y, Zhao X, Yu X, et al. (2014) Nanosized TiO2 Exposure Resulted in Neurotoxicity via Impairing NMDA Receptor-mediated Postsynaptic Signaling Cascade in Mice. J Nanomed Nanotechnol 5:203. doi:10.4172/2157-7439.1000203

Copyright: © 2014 Sheng L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The central nervous system (CNS) toxicity induced by exposure to nano-sized particles is of great concern, but the mechanism of how this toxicity may be incurred has yet to be elucidated. Here, we examined how N-methyl-D-aspartate (NMDA) receptor-mediated postsynaptic signalling cascade may be affected by titanium dioxide particles (TiO2 NPs) exposure for six consecutive months to contribute to the observed neurotoxicity. The results suggest that long-term exposure to TiO2 NPs led to titanium accumulation and iron reduction in the blood and hippocampus tissues, and significant hippocampal injury as well as reduction of learning and memory in mice. The CNS injuries following longterm TiO2 NP exposure were closely associated with significant reductions in NR1, NR2A, NR2B, calcium/calmodulindependent protein kinase II, postsynaptic density protein 95, nuclear activated extracellular-signal regulated kinase (ERK1/2), Dexras1, CAPON, peripheral benzodiazepine receptor-associated protein, and divalent metal transporter as well as elevation of synaptic Ras GTPase- activating protein and neural nitric oxide synthase in the hippocampus. It implies that long-term exposure to TiO2 NPs may induce neurotoxic effects via impairing NMDA receptor-mediated postsynaptic signalling cascade in animals.

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