Data include: trans-epithelial electrical resistance, FITC-dextran permeability, cell viability and gene expression (RNA and protein). This dataset is associated with the following publication: Faber, S., N. McNabb, P. Ariel, E. Aungst, and S. McCullough. Exposure Effects Beyond the Epithelial Barrier: Trans-Epithelial Induction of Oxidative Stress by Diesel Exhaust Particulates in Lung Fibroblasts in an Organotypic Human Airway Model. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 177(1): 140-155, (2020).

Data corresponding to figures contained in manuscript. This dataset is associated with the following publication: Masood, S., E. Pennington, S. Simmons, P. Bromberg, S. Shaikh, R. Rice, A. Gold, Z. Zhang, and J. Samet. Live cell imaging of oxidative stress in human airway epithelial cells exposed to isoprene hydroxyhydroperoxide. Redox Biology. Elsevier B.V., Amsterdam, NETHERLANDS, 51: 102281, (2022).

Pulmonary gene expression related to the regulation of DNA methylation following an exposure to ozone in rats. Epigenetic regulation of a pulmonary hypertensive gene, apelin, was also quantified. This dataset is associated with the following publication: Miller, C., J. Dye, M. Schladweiler, J. Richards, A. Ledbetter, E. Stewart, and U. Kodavanti. Acute inhalation of ozone induces DNA methylation of apelin in lungs of Long-Evans rats.. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 30(4): 178-186, (2018).

Data corresponding to the figures in this article. This dataset is associated with the following publication: Corteselli, E., J. Samet, and E. Gibbs-Flournoy. IMAGING APPROACHES TO ASSESSMENTS OF TOXICOLOGICAL OXIDATIVE STRESS USING GENETICALLY ENCODED FLUOROGENIC SENSORS. Journal of Visualized Experiments. JoVE, Somerville, MA, USA, 132: 56945, (2018).

This data set contains one Excel file. In this file are all the data pertaining to the effects of propranolol and mifepristone on ozone induced lung injury and inflammation . The different tabs of the spreadsheet pertain to each figure found in the manuscript. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, J. Richards, K. Mauge-Lewis, M. McGee, and U. Kodavanti. Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 339: 161-171, (2018).

This data set pertains to the manuscript "Exacerbation of ozone-induced pulmonary and systemic effects by 2-adrenergic and/or glucocorticoid agonist/s". It shows the raw data for each figure in the manuscript that is created with these data. Basically examining the influence of beta adrenergic and glucocorticoid receptor agonists on ozone-induced lung injury and inflammation. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, M. Hargrove, U. Kodavanti, and J. Richards. Exacerbation of ozone-induced pulmonary and systemic effects by beta2-adrenergic and/or glucocorticoid agonist/s. Scientific Reports. Nature Publishing Group, London, UK, 9(1): 17925, (2019).

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 filtered 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. Diet seemed to be the driving factor in most OS measures. Overall, OS parameters measured do not suggest a consistent O3/diet interaction on oxidative damage pathways, but do give insight as to how high caloric diets could affect neuronal OS. This dataset is associated with the following publication: Valdez, J., A. Johnstone, J. Richards, J. 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 AG, Basel, SWITZERLAND, 1-17, (2018).

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 filtered 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. Diet seemed to be the driving factor in most OS measures. Overall, OS parameters measured do not suggest a consistent O3/diet interaction on oxidative damage pathways, but do give insight as to how high caloric diets could affect neuronal OS. This dataset is associated with the following publication: Valdez, J., A. Johnstone, J. Richards, J. 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 AG, Basel, SWITZERLAND, 1-17, (2018).

This data set is an excel file pertaining to the study that examined ozone-induced systemic and pulmonary effects in rats that underwent SHAM surgery (control), adrenal demedullation or total bilateral adrenalectomy. Different pages of the spreadsheet shows individual animal data for markers of lung injury and inflammation, body weights, whole body plethysmography measurements, levels of circulating hormones and lipids, and circulating white blood cell count as well as platelet count. This dataset is associated with the following publication: Miller, D., S. Snow, M. Schladweiler , J. Richards , A. Ghio , A. Ledbetter , and U. Kodavanti. Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects are Diminished in Adrenalectomized Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 150(2): 312-22, (2016).

This data set is an excel file pertaining to the study that examined ozone-induced systemic and pulmonary effects in rats that underwent SHAM surgery (control), adrenal demedullation or total bilateral adrenalectomy. Different pages of the spreadsheet shows individual animal data for markers of lung injury and inflammation, body weights, whole body plethysmography measurements, levels of circulating hormones and lipids, and circulating white blood cell count as well as platelet count. This dataset is associated with the following publication: Miller, D., S. Snow, M. Schladweiler , J. Richards , A. Ghio , A. Ledbetter , and U. Kodavanti. Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects are Diminished in Adrenalectomized Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 150(2): 312-22, (2016).