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The Effects of Ozone Exposure and Sedentary Lifestyle on Neuronal Microglia and Mitochondrial Bioenergetics of Female Long-Evans Rats
Citation:
Valdez, M., J. Valdez, D. Freeborn, A. Johnstone, AND P. Kodavanti. The Effects of Ozone Exposure and Sedentary Lifestyle on Neuronal Microglia and Mitochondrial Bioenergetics of Female Long-Evans Rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, 408:115254, (2020). https://doi.org/10.1016/j.taap.2020.115254
Impact/Purpose:
Epidemiological data suggest that sedentary lifestyles may exacerbate responses to air pollutants such as O3. We sought to assess neurological changes in response to O3 exposure and an active lifestyle. Microglia and astrocytes play critical roles in the maintenance and functioning of the central nervous system (CNS). Astrocytes work intimately with neurons in sustaining functioning synapses as well as preserving the blood brain barrier. Microglia act as sentinels within the CNS. Mitochondria are key regulators of cellular energy homeostasis and may play a key role in the mechanisms of neurodegenerative disorders and chemical induced neurotoxicity. We developed an animal model in which female Long-Evans rats were either sedentary or active with continuous access to running wheels starting at postnatal day (PND) 22 until the age of PND 100 and then exposed to O3 (0, 0.25, 0.5 or 1.0 ppm) 5 h/day for two consecutive days. We found that O3 and exercise interact to produce region specific alterations in mitochondrial bioenergetics in the frontal cortex, cerebellum, hippocampus and hypothalamus. Additionally, we found that O3 induces microglia reactivity within stress centers of the brain and that mitochondrial bioenergetics are altered. Some of these effects may be mitigated by exercise, suggesting a significant role of lifestyle in O3 effects on brain mitochondrial bioenergetics parameters.
Description:
Ozone (O3) is a widespread air pollutant that produces cardiovascular and pulmonary dysfunction possibly mediated by activation of central stress centers. Epidemiological data suggest that sedentary lifestyles may exacerbate responses to air pollutants such as O3. We sought to assess neurological changes in response to O3 exposure and an active lifestyle. We developed an animal model in which female Long-Evans rats were either sedentary or active with continuous access to running wheels starting at postnatal day (PND) 22 until the age of PND 100 and then exposed to O3 (0, 0.25, 0.5 or 1.0 ppm) 5 h/day for two consecutive days. We found significantly more reactive microglia within the hippocampus (HIP) in animals exposed to O3 in both sedentary and active rats. No changes were detected in astrocytic coverage. We next analyzed mitochondrial bioenergetic parameters (complex I, complex II and complex IV). Complex I activity was significantly affected by exercise in hypothalamus (HYP). Complex II activity was significantly affected by both exercise and O3 exposure in the HIP. Concomitant with the changes in enzymatic activity, there were also effects on expression of genes related to mitochondrial bioenergetics and antioxidant production. These results demonstrate that O3 induces microglia reactivity within stress centers of the brain and that mitochondrial bioenergetics are altered. Some of these effects may be augmented by exercise, suggesting a role for lifestyle in O3 effects on brain mitochondrial bioenergetics parameters in agreement with our previous reports on other endpoints.
URLs/Downloads:
DOI: The Effects of Ozone Exposure and Sedentary Lifestyle on Neuronal Microglia and Mitochondrial Bioenergetics of Female Long-Evans Rats