Citation:

Valdez, J., A. Johnstone, J. Richards, Judy Schmid, J. Royland, AND P. Kodavanti. Interaction of Diet and Ozone Exposure on Oxidative Stress Parameters within Specific Brain Regions of Male Brown Norway Rats. International Journal of Molecular Sciences. MDPI, Basel, Switzerland, 20(1):11, (2019). https://doi.org/10.3390/ijms20010011

Impact/Purpose:

This article addresses the potential effects of dietary induced obesity on the susceptibility to ozone exposure, and specifically, possible adverse effects or interactions in regards to oxidative stress pathways in specific brain regions. Diets rich in fructose and fat are considered to be major risk factors leading to obesity. In addition, obesity is considered to be a risk factor that increases air pollution susceptibility. We conclude that rats given these calorie dense diets did not have a propensity for increased neuronal oxidative stress with ozone exposure. However, there were diet specific interactions with oxidative stress pathways when compared to control diet, which may give insight into diet effects on neurodegenerative diseases and oxidative stress.

Description:

Oxidative stress (OS) is a contributing factor to the neuro, cardiac, and pulmonary effects caused by adverse metabolic states, such as obesity and type II diabetes, as well as inhalation of air borne toxicants, such as ozone (O3). The objective of this study is to understand diet/O3 interactions on OS parameters in young male Brown Norway rats maintained on regular (Purina 5001), high fructose (FRUC, TD.89247), or high fat (FAT, TD.06414) diet for 16 wks followed by exposure to either filtered air or 0.8 ppm O3 under an acute (1 d for 5 h) or subacute (5 h/d, 1 d/wk for four wks) paradigm. After 18 h of the last exposure, measures of ROS production (NAD(P)H:quinone oxidoreductase (NQO1) and NADH-Ubiquinone reductase (UBIQ-RD) levels), antioxidant homeostasis (total antioxidant substance (TAS) and γ-Glutamylcysteine synthetase (gGCS) activity), and oxidative damage (total aconitase activity and protein carbonyl (PC) content) were assayed in selected brain regions. Diet/O3 interaction did not have a global effect in the brain, but did show limited regional and OS parameter specific effects. HIP showed a significant interaction between FRUC diet/O3. Aconitase in CER showed a significant interaction between diet and O3. However, regional effects of either O3 or diet alone were more profound. Within the acute condition, there was a decrease in NQ01 and UBIQ-RD in STR and HIP, respectively, regardless of exposure. Also, CER and STR showed a change in TAS due to diet alone, while FC seemed to have a larger amount of TAS due to O3 alone. Diet appeared to affect gGCS negatively in all diet groups of HIP, and only in the FAT diet of STR. The CER also appear to have a decrease in PC in FRUC group and a general decrease in PC in all diets due to O3, while aconitase increased only in FRUC air exposed animals and control O3 exposed animals. Under the subacute condition, there was an increase of NQO1 activity in only the CER due to diets alone, while UBIQ-RD increased in only the FRUC group in FC and in both diet groups in HIP. TAS was decreased in FC only in the FAT group and a clear O3 effect where FAT increased the TAS and FRUC decreased in TAS. A significant interaction between diet/O3 was found in FC. The STR also showed a decrease in TAS in response to O3. Diet also increased PC formation within CER only in the FAT group, while HIP showed a decrease in PC after O3 exposure in controls. Aconitase in CER was affected both by diet in the air group while O3 caused a decrease in controls and FRUC groups. O3 affected all groups within HIP and HYP. STR was most affected by FAT diet in both air and O3 groups. Overall, diet seemed to be the driving factor in most OS measures. Overall, oxidative stress parameters measured do not suggest a consistent ozone/diet interaction on oxidative damage pathways, but do give insight as to how high caloric diets could affect neuronal oxidative stress.

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