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  4. Effects of zinc oxide nanoparticles exposure on central nervous system in Sprague-Dawley rats
 
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Effects of zinc oxide nanoparticles exposure on central nervous system in Sprague-Dawley rats

Date Issued
2016
Date
2016
Author(s)
Yang, Yu-Ting
DOI
10.6342/NTU201602331
URI
http://ntur.lib.ntu.edu.tw//handle/246246/277324
Abstract
With the rapid development of nanotechnology, nanomaterials have been used widely in human life. Studies have shown that nanomaterials have greater toxicity than larger particles on the same masses. Zinc oxide as one of the most important and useful nanomaterials, have been widely applied in commercial products. Thus, the potential toxicity of zinc oxide has become an important issue. Many researchers have explored the respiratory toxicity of ZnO-NPs. However, few studies investigated central nervous system toxicity of ZnO-NPs. Previous studies showed that ZnO-NPs might impair spatial learning ability in rats, however, the outcome was inconsistent. Thus, the aim of our study is to explore central nervous system toxicity and the underlying mechanisms induced by ZnO-NPs. In our present study, 8-week-old Sprague-Dawley rats were exposed to ZnO-NPs at the dose of 5 mg/kg, 10 mg/kg and 20 mg/kg respectively via intratracheal instillation (IT). One group (N=5) was sacrificed 24 hrs after the exposure to ZnO-NPs. We collected brain tissue including hippocampus, cerebellum and cortex to analyze proinflammatory cytokines, oxidative stress, nitrative stress and zinc content. Another group (N=10) underwent morris water maze and elevated-plus maze for 5 days. In the next day, rats were sacrificed and the brain and lung tissue were collected for pathological examination. Our results showed that ZnO-NPs exposure didn’t affect spatial learning ability and anxiety. Results showed that ZnO-NPs exposure caused decreased cytokine level in high dose such as IL-1α in hippocampus, IL-1β, IL-6 and TNF-αin cerebellum and IL-1α、IL-1βand IL-6 in cortex. Oxidative stress marker 8-OHdG increased in hippocampus and cerebellum. There was no difference between groups for 8-NO2Gua. Zinc levels increased in cerebellum but not in cortex. Histology examination showed a dose-response inflammation in lung. However, there was no changes in brain. We conclude that zinc might play an important role in central nervous system toxicity caused by ZnO-NPs. Zinc cause a decrease in cytokines and an increase in oxidative stress, but the effects are not consistent through brain regions. Cerebellum seems vulnerable to ZnO-NPs. Our study sheds some light on the possible mechanisms and effects caused by ZnO-NPs, however, the exact mechanisms required further study.
Subjects
Morris Water Maze
Elevated-plus maze
Zinc oxide nanoparticle
Central nervous system
spatial learning and memory
Zinc
Oxidative stress
Type
thesis
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