Xinxin Ding

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Journals/Publications

• Zhang, Q. Y., Winkle, L. V., Kovalchuk, N., & Ding, X. (2020). Contribution of Pulmonary CYP-mediated Bioactivation of Naphthalene to Airway Epithelial Injury in the Lung.. Toxicological sciences : an official journal of the Society of Toxicology, 177(2), 334-346. doi:10.1093/toxsci/kfaa114
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  Previous studies have established that cytochrome P450 enzymes (CYPs) in both liver and lung are capable of bioactivating naphthalene (NA), an omnipresent air pollutant and possible human carcinogen, in vitro and in vivo. The aim of this study was to examine the specific contribution of pulmonary CYPs in airway epithelial cells to NA-induced airway toxicity. We used a lung-Cpr-null mouse model, which undergoes doxycycline-induced, Cre-mediated deletion of the Cpr (a redox partner of all microsomal CYPs) gene specifically in airway epithelial cells. In 2-month-old lung-Cpr-null mice, Cpr deletion occurred in 75%-82% of epithelial cells of conducting airways. The extent of NA-induced acute lung toxicity (as indicated by total protein concentration and lactate dehydrogenase activity in bronchoalveolar lavage fluid collected at 24-h after initiation of a 4-h, nose-only, 10-ppm NA inhalation exposure) was substantially lower (by 37%-39%) in lung-Cpr-null mice, compared with control littermates. Moreover, the extent of cellular proliferation (as indicated by 5-bromo-2'-deoxyuridine incorporation) was noticeably lower in both proximal and distal airways (by 59% and 65%, respectively) of NA-treated lung-Cpr-null mice, compared with control littermates, at 2-day post-NA inhalation exposure. A similar genotype-related difference in the extent of postexposure cell proliferation was also observed in mice exposed to NA via intraperitoneal injection at 200 mg/kg. These results directly validate the hypothesis that microsomal CYP enzymes in airway epithelial cells play a large role in causing injury to airway epithelia following exposure to NA via either inhalation or intraperitoneal route.
• Buchholz, B. A., Carratt, S. A., Kuhn, E. A., Collette, N. M., Ding, X., & Van, W. (2019). Naphthalene DNA adduct formation and tolerance in the lung. NUCLEAR INSTRUMENTS & METHODS IN PHYSICS RESEARCH SECTION B-BEAM INTERACTIONS WITH MATERIALS AND ATOMS, 438, 119-123.
• Carratt, S. A., Hartog, M., Buchholz, B. A., Kuhn, E. A., Collette, N. M., Ding, X., & Van, W. (2019). Naphthalene genotoxicity: DNA adducts in primate and mouse airway explants. TOXICOLOGY LETTERS, 305, 103-109.
• Carratt, S. A., Kovalchuk, N., Ding, X., & Van, W. (2019). Metabolism and Lung Toxicity of Inhaled Naphthalene: Effects of Postnatal Age and Sex. TOXICOLOGICAL SCIENCES, 170(2), 536-548.
• Fan, X., Li, H., Ding, X., & Zhang, Q. (2019). Contributions of Hepatic and Intestinal Metabolism to the Disposition of Niclosamide, a Repurposed Drug with Poor Bioavailability. DRUG METABOLISM AND DISPOSITION, 47(7), 756-763.
• Hartog, M., Zhang, Q., & Ding, X. (2019). Role of Mouse Cytochrome P450 Enzymes of the Cyp2abfgs Subfamilies in the Induction of Lung Inflammation by Cigarette Smoke Exposure. TOXICOLOGICAL SCIENCES, 172(1), 123-131.
• Kovalchuk, N., Zhang, Q., Kelty, J., Van, W. L., & Ding, X. (2019). Toxicokinetic Interaction between Hepatic Disposition and Pulmonary Bioactivation of Inhaled Naphthalene Studied Using Cyp2abfgs-Null and CYP2A13/2F1-Humanized Mice with Deficient Hepatic Cytochrome P450 Activity. DRUG METABOLISM AND DISPOSITION, 47(12), 1469-1478.
• Wang, H., Qin, M., Liu, R., Ding, X., Chen, I., & Jiang, Y. (2019). Characterization of A Bifunctional Synthetic RNA Aptamer and A Truncated Form for Ability to Inhibit Growth of Non-Small Cell Lung Cancer. SCIENTIFIC REPORTS, 9.
• Zhang, Y. u., Shen, B., Guan, X., Qin, M., Ren, Z., Ma, Y., Dai, W., Ding, X., & Jiang, Y. (2019). Safety and efficacy of ex vivo expanded CD34(+) stem cells in murine and primate models. STEM CELL RESEARCH & THERAPY, 10.