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. 2019 Aug 12;9:11613. doi: 10.1038/s41598-019-48006-6

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© The Author(s) 2019

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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Hypoxia/Reoxygenation induced AC16 cells death. AC16 cells were subjected to hypoxia 5 h (1% O₂, PBS) and reoxygenation 1 h (21% O₂, DMEM) (H/R). (a) Viability (MTT) significantly decreased in H/R versus normoxic CTL, n = 8. (b) Intracellular ATP, a reflect of cell health, significantly decreased in H/R versus normoxic CTL, n = 8. (c) Cell death assessed by LDH release significantly increased in H/R versus normoxic CTL, n = 8. Data are given as relative mean ± s.e.m. (d) Oxygen consumption in non-permeabilized cells after 5 h/1 h H/R at basal state (Routine), state 4 (Leak) and maximal electron transport chain activity (ETS capacity) were significantly decreased compared to CTL. n = 4. ETS, electron transport system; *p < 0.05; **p < 0.01 from control condition (CTL).