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. 2022 Oct 25;28(1-2):186–198. doi: 10.1007/s10495-022-01775-4

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Analysis of ROS and DNA damage upon LACTB induction. (A) Immunofluorescence for γ-H2AX in MCF7ras. Images were taken with a Zeiss LSM 780 confocal microscope from a middle section of the cells. γ-H2AX-positive cells were counted, and averages ± SD from different experiments are shown on the right graph. (B) Flow cytometry analysis of general ROS production after LACTB induction. (C) Flow cytometry analysis of mitochondrial ROS superoxide by MitoSOX. (D) Flow cytometry analysis of ROS-mediated DNA damage by 8-OHdG detection. (E) Cell proliferation assay with the antioxidant NAC and LACTB overexpression. Values are represented as the average ± SD of three independent experiments. *P < 0,05; **P < 0,01; ***P < 0,001. Scale bar: 10 μm