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. 2019 Oct 29;9:15547. doi: 10.1038/s41598-019-52107-7

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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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CKD mice experience severe skeletal muscle mitochondriopathy in the ischemic limb. Mitochondrial function was assessed in situ using permeabilized myofiber bundles prepared from the gastrocnemius muscles. (A) Mitochondrial respiratory function under numerous substrate conditions was significantly decreased in the ischemic muscle of CKD mice. (B) Mitochondrial hydrogen peroxide emission was slightly, but not statistically, elevated in CKD mice. (C) Calculated hydrogen peroxide buffering capacity (percent increase in H₂O₂ emission with auranofin) was lower in CKD mice. (D) Electron leak (JH₂O₂/JO₂) supported by succinate (state 2) was also higher in CKD mice. *P < 0.05 vs. control mice. ^aP < 0.05 vs. non-ischemic control (within group), ^bP < 0.05 vs. control mice (between group, same limb) using ANOVA with Tukey’s post-hoc testing. N = 5/group. Error bars represent SEM. FAL = femoral artery ligation.