Difference between revisions of "Salvi 2019 Neurobiol Stress"
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{{Publication | {{Publication | ||
|title=Salvi A, Liu H, Salim S ( | |title=Salvi A, Liu H, Salim S (2019) Involvement of oxidative stress and mitochondrial mechanisms in air pollution-related neurobiological impairments. Neurobiol Stress 12:100205. | ||
|info=[https://www.sciencedirect.com/science/article/pii/S2352289519300578 Open Access] | |info=[https://www.sciencedirect.com/science/article/pii/S2352289519300578 Open Access] | ||
|authors=Salvi A, Liu H, Salim S | |authors=Salvi A, Liu H, Salim S | ||
|year= | |year=2019 | ||
|journal=Neurobiol Stress | |journal=Neurobiol Stress | ||
|abstract=Vehicle exhaust emissions are known to be significant contributors to physical and psychological stress. Vehicle exhaust-induced stress and associated respiratory and cardiovascular complications are well-known, but the impact of this stress on the brain is unclear. Simulated vehicle exhaust exposure (SVEE) in rats causes behavioral and cognitive deficits. In the present study, the underlying mechanisms were examined. Our postulation is that SVEE, a simulation of physiologically relevant concentrations of pro-oxidants (0.04% carbon dioxide, 0.9 ppm nitrogen dioxide, 3 ppm carbon monoxide) creates a toxic stress environment in the brain that results in an imbalance between production of reactive oxygen species and the counteracting antioxidant mechanisms. This impairs mitochondrial function in the high bioenergetic demand areas of the brain including the hippocampus (HIP), amygdala (AMY) and the prefrontal cortex (PFC), disrupting neuronal network, and causing behavioral deficits. Mitochondria-targeted antioxidant Mito-Q protects against these impairments. | |abstract=Vehicle exhaust emissions are known to be significant contributors to physical and psychological stress. Vehicle exhaust-induced stress and associated respiratory and cardiovascular complications are well-known, but the impact of this stress on the brain is unclear. Simulated vehicle exhaust exposure (SVEE) in rats causes behavioral and cognitive deficits. In the present study, the underlying mechanisms were examined. Our postulation is that SVEE, a simulation of physiologically relevant concentrations of pro-oxidants (0.04% carbon dioxide, 0.9 ppm nitrogen dioxide, 3 ppm carbon monoxide) creates a toxic stress environment in the brain that results in an imbalance between production of reactive oxygen species and the counteracting antioxidant mechanisms. This impairs mitochondrial function in the high bioenergetic demand areas of the brain including the hippocampus (HIP), amygdala (AMY) and the prefrontal cortex (PFC), disrupting neuronal network, and causing behavioral deficits. Mitochondria-targeted antioxidant Mito-Q protects against these impairments. |
Latest revision as of 12:31, 13 January 2020
Salvi A, Liu H, Salim S (2019) Involvement of oxidative stress and mitochondrial mechanisms in air pollution-related neurobiological impairments. Neurobiol Stress 12:100205. |
Salvi A, Liu H, Salim S (2019) Neurobiol Stress
Abstract: Vehicle exhaust emissions are known to be significant contributors to physical and psychological stress. Vehicle exhaust-induced stress and associated respiratory and cardiovascular complications are well-known, but the impact of this stress on the brain is unclear. Simulated vehicle exhaust exposure (SVEE) in rats causes behavioral and cognitive deficits. In the present study, the underlying mechanisms were examined. Our postulation is that SVEE, a simulation of physiologically relevant concentrations of pro-oxidants (0.04% carbon dioxide, 0.9 ppm nitrogen dioxide, 3 ppm carbon monoxide) creates a toxic stress environment in the brain that results in an imbalance between production of reactive oxygen species and the counteracting antioxidant mechanisms. This impairs mitochondrial function in the high bioenergetic demand areas of the brain including the hippocampus (HIP), amygdala (AMY) and the prefrontal cortex (PFC), disrupting neuronal network, and causing behavioral deficits. Mitochondria-targeted antioxidant Mito-Q protects against these impairments.
• Bioblast editor: Plangger M
Labels: MiParea: Respiration, mt-Structure;fission;fusion, Comparative MiP;environmental MiP
Stress:Oxidative stress;RONS Organism: Rat Tissue;cell: Nervous system Preparation: Isolated mitochondria
Regulation: ATP production
HRR: Oxygraph-2k
Labels, 2020-01