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. 2019 Sep 24;9:13748. doi: 10.1038/s41598-019-50141-z

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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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Effects of IA on mitochondrial bioenergetics, transmembrane potential and ROS production. (A) The Seahorse mito-stress assay. OCR is measured before and after adding inhibitors/uncoupler to induce different mitochondrial respiratory states (defined in the shaded areas). (B) Basal respiration, proton leak, spare capacity, and non-mitochondrial respiratory rates (defined in A) were quantified and compared for both cell types after 4 or 12 h of treatment with 20 mM IA. (C,D) Effect of IA-treatment time on mitochondrial transmembrane potential as determined by flow cytometric analysis using TMRE staining for both MCF7 and MDA-MB-231 cells; respectively. (E,F) Flow cytometric analysis of cellular ROS levels using DCF cellular staining of both MCF7 and MDA-MB-231 cells; respectively.