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. 2020 Apr 22;10:6846. doi: 10.1038/s41598-020-63761-7

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Mitochondrial reactive species generated during chronic intermittent hypoxia (IH) exposure in preadipocytes is attenuated in presence of aspirin, atorvastatin and drugs targeting renin-angiotensin system. Intervention with aspirin, atorvastatin, angiotensin II type-1 receptor antagonist (losartan), and angiotensin converting enzyme inhibitor (captopril) reduced IH-induced mitochondrial reactive oxygen species generation while angiotensinII (AngII) increased mitochondrial reactive oxygen species generation as indicated by MitoSox staining (a) Representative images of MitoSox staining with red color indicating increased ROS (b). Cells treated with menadione (150 µM) served as a positive control and cells treated with N-acetyl-L-cysteine (50 µM) served as a negative control. Data are presented as mean ± SEM, *P < 0.05 determined by one-tailed paired t-test (n = 3–5 independent experiments) as compared to IH. NO: normoxia.