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Corteselli et al. JoVE Science Hub Data
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).
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Live Cell Imaging of Oxidative Stress in Human Airway Epithelial Cells Exposed to Isoprene Hydroxy Hydroperoxide METADATA
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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).
PISCES lung dataset
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This dataset contains ambient air pollution data during the study period and lung function and biomarkers data. This dataset is associated with the following publication: Tong, H., S. Zhang, W. Shen, H. Chen, C. Salazar, A. Schneider, A. Rappold, D. Diaz-Sanchez, R. Devlin, and J. Samet. Lung Function and Short-Term Ambient Air Pollution Exposure: Differential Impacts of Omega-3 and Omega-6 Fatty Acids. Annals of the American Thoracic Society. American Thoracic Society, New York, NY, USA, 19(4): 583-593, (2022).
Corteselli et al Ozone PUFA Ox Stress
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These are the data for the figures in the manuscript. This dataset is associated with the following publication: Corteselli, E., A. Gold, J. Surratt, T. Cui, P. Bromberg, L. Dailey, and J. Samet. Supplementation with Omega-3 Fatty Acids Potentiates Oxidative Stress in Human Airway Epithelial Cells Exposed to Ozone. ENVIRONMENTAL RESEARCH. Elsevier B.V., Amsterdam, NETHERLANDS, 187: 109627, (2020).
Adaptations of HAEC to ISOPOOH - METADATA v1 112522
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This metadata excel file contains the primary data collected for this project. Each sheet represents the data that corresponds to each individual figure and supplemental data set. This dataset is associated with the following publication: Pennington, E., S. Masood, S. Simmons, L. Dailey, P. Bromberg, R. Rice, A. Gold, Z. Zhang, W. Wu, Y. Yang, and J. Samet. Real-Time Redox Adaptations in Human Airway Epithelial Cells Exposed to Isoprene Hydroxy Hydroperoxide. Redox Biology. Elsevier B.V., Amsterdam, NETHERLANDS, 61(102646): 1, (2023).
Identifying Trans-Epithelial Effects of Inhaled Chemical Exposures on Stromal-Epithelial Oxidative Stress Dynamics in the Human Airway
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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).
Cytotoxicity and Oxidative Stress Induced by Atmospheric Mono-Nitrophenols in Human Lung Cells
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GC-MS chromatograms of silylated samples from the photooxidation of toluene in the presence of NOx showing the secondary origin of nitrophenols. This dataset is associated with the following publication: Khan, F., M. Jaoui, K. Rudziński, K. Kwapiszewska, A. Martinez-Romero, D. Gil-Casanova, M. Lewandowski, T. Kleindienst, J. Offenberg, J.D. Krug, J. Surratt, and R. Szmigielski. Cytotoxicity and Oxidative Stress Induced by Atmospheric Mono-Nitrophenols in Human Lung Cells. ENVIRONMENTAL POLLUTION. Elsevier Science Ltd, New York, NY, USA, 301(15): 119010, (2022).
burnpit computational data
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meta data. This dataset is associated with the following publication: Kim, Y.H., J. Rager, I. jaspers, and M. Gilmour. Computational Approach to Link Chemicals in Anthropogenic Smoke Particulate Matter with Toxicity. CHEMICAL RESEARCH IN TOXICOLOGY. American Chemical Society, Washington, DC, USA, 35(12): 2210-2213, (2022).
E320 Diet Ozone Oxidative Stress Data
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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).
Seahorse Manuscript Data Set
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Metadata for figures presented in manuscript reporting bioenergetic effects of exposure to environmentally relevant organic compound in human airway epithelial cells. This dataset is associated with the following publication: Lavrich, K., E. Corteselli, P. Wages, P. Bromberg, S. Simmons, E. Gibbs-Flournoy, and J. Samet. Investigating Mitochondrial Dysfunction in Human Lung Cells Exposed to Redox-Active PM Components. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 342: 99-107, (2018).
CDDP hypersensitivity Science Hub Data.xlxs
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Excel file contains data used to generate figures and tables. This dataset is associated with the following publication: Lehmann, D., and W. Williams. Physiological Responses to Cisplatin Using a Mouse Hypersensitivity Model. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 32(2): 68-78, (2020).