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. 2020 Jun 30;10:10665. doi: 10.1038/s41598-020-67812-x

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© The Author(s) 2020

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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Impact of GCN5L1 deletion on ROS regulation and damage in response to a HFD. (A, B) Acetylation of superoxide dismutase 2 (SOD2) at K122 is significantly increased in whole cardiac tissue from WT animals in response to a HFD. There was no increase in SOD2 acetylation in GCN5L1 cKO mice under the same dietary conditions. (C) Cardiac lipid peroxidation in samples obtained from while cardiac tissue, a measure of ROS damage, is significantly lower in GCN5L1 cKO mice relative to WT mice under HFD conditions. Values are expressed as means ± SD, n = 4–8, *P < 0.05 versus WT LFD, ^#P < 0.05 versus WT HFD.