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. 2022 May 10;19:33. doi: 10.1186/s12989-022-00467-w

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — CuO NPs trigger lysosomal acidification. a RAW264.7 macrophages were labeled using LysoSensor™ Green following exposure to CuO NPs (25 µg/mL) for 6 h and visualized by confocal microscopy. Scale bars: 10 µm. b LysoSensor™ Green fluorescence in control cells and cells exposed to CuO NPs (25 µg/mL) was determined by flow cytometry. Preincubation with bafilomycin A1 (10 nM) (c) and TTM (50 µM) (d) protected the RAW264.7 macrophages from CuO NP-triggered cell death as shown using the Alamar blue assay. Data are mean values ± S.D. (n = 3). **p < 0.01; ***p < 0.001; ****p < 0.0001 (significant difference between control and treatments); ^#p < 0.05; ^###p < 0.001 (significant difference between treatments)