PM2.5, SO2 and NO2 co-exposure impairs neurobehavior and induces mitochondrial injuries in the mouse brain.
In: Chemosphere, Jg. 163 (2016-11-15), S. 27-34
academicJournal
Zugriff:
Air pollution is a serious environmental health problem that has been previously associated with neuropathological disorders. However, current experimental evidence mainly focuses on the adverse effects of a single air pollutant, ignoring the biological responses to the co-existence of these pollutants. In the present study, we co-exposed C57BL/6 J mice to PM 2.5 , SO 2 and NO 2 and explored their neurobehavior, histopathologic abnormalities, apoptosis-related protein expression and mitochondrial dysfunction. The results indicate that co-exposure to PM 2.5 , SO 2 and NO 2 impaired spatial learning and memory and caused abnormal expression of apoptosis-related genes (p53, bax and bcl-2). Additionally, these alterations were related to morphological changes in mitochondria, a reduction of ATP, the elevation of mitochondrial fission proteins and the downregulation of fusion proteins. These findings provide a basis for the understanding of mitochondrial abnormality-related neuropathological dysfunction in response to co-exposure to ambient air pollutants, which suggests an adaptive response to the frangibility of the central nerve system. [ABSTRACT FROM AUTHOR]
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PM2.5, SO2 and NO2 co-exposure impairs neurobehavior and induces mitochondrial injuries in the mouse brain.
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Autor/in / Beteiligte Person: | Ku, Tingting ; Ji, Xiaotong ; Zhang, Yingying ; Li, Guangke ; Sang, Nan |
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Zeitschrift: | Chemosphere, Jg. 163 (2016-11-15), S. 27-34 |
Veröffentlichung: | 2016 |
Medientyp: | academicJournal |
ISSN: | 0045-6535 (print) |
DOI: | 10.1016/j.chemosphere.2016.08.009 |
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