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. 2022 May 2;14(9):2272. doi: 10.3390/cancers14092272

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Nicotine- or cotinine-reduced SCLC sensitivity towards cisplatin-induced DNA damage by regulating cellular redox metabolism. (A–C) Reactive oxygen species (ROS) analysis suggesting that cisplatin-induced cellular ROS could be completely blocked by nicotine or cotinine exposure while cisplatin and nicotine or cotinine co-treatment significantly induces the production of GSH and NADPH in SCLC cells. (D–F) The effects of nicotine or cotinine on ROS, GSH, and NADPH in DMS53, with or without cisplatin treatment. (G–I) The effects of nicotine or cotinine on ROS, GSH, and NADPH in H146, with or without cisplatin treatment. (J–O) The effects of nicotine or cotinine on ROS, GSH, and NADPH in H841 and DMS53, with or without etoposide treatment. (P) The effects of cotinine exposure on the expression levels of NRF2 target genes. Statistically significant differences determined using two-tailed student t test. *, p < 0.05; **, p < 0.01; ***, p < 0.001.