Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6306276 | Chemosphere | 2016 | 8 Pages |
Abstract
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/6Â J mice to PM2.5, SO2 and NO2 and explored their neurobehavior, histopathologic abnormalities, apoptosis-related protein expression and mitochondrial dysfunction. The results indicate that co-exposure to PM2.5, SO2 and NO2 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.
Keywords
PBSMFNFis1Drp1PM2.5BSAopa1NOxoptic atrophy 1bovine serum albuminAir pollutantNeuronal apoptosissodium dodecyl sulfate-polyacrylamide gel electrophoresisSDS-PAGENitrogen oxidesTemSulfur dioxideSO2Fine particulate matterphosphate buffer salineMitofusinTransmission electron microscopyNitrocelluloseCo-exposurehematoxylin-eosindynamin-related protein 1Spatial learning and memory
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Environmental Chemistry
Authors
Tingting Ku, Xiaotong Ji, Yingying Zhang, Guangke Li, Nan Sang,