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. 2022 Dec 12;12:21483. doi: 10.1038/s41598-022-25802-1

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© The Author(s) 2022

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 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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PON2 depletion impairs mitochondrial metabolism and oxidative stress. (a) Seahorse measurement of oxygen consumption rate (OCR) in PON2-deficient and control cells treated with or without PA. (b) Bar plots of maximal OCR and spare respiratory capacity are shown. Data were obtained from three independent experiments. (c) Confocal fluorescence images showing the generation of mitochondrial superoxide, which was analyzed using MitoSox. PON2-deficient and control cells were treated with or without PA for 24 h and stained with MitoSox. Cell nuclei were stained with Hoechst 33342. Representative images from three independent experiments are shown above (scale bar = 50 μm). (d) Bar plots of the MitoSox staining intensity are shown below. (e) Immunoblotting analysis of phosphorylation of JNK1/2 as marker for mitochondrial oxidative stress in PON2-deficient and control cells. ACTB was used as a loading control. Band intensities of indicated proteins are shown below. (f) The expression of genes related to mitochondrial electron transfer chain in PON2-deficient cells relative to controls. Bar plots of the average expression of genes are shown. (g) The expression of genes related to mitochondrial TCA cycle in PON2-deficient cells relative to controls.