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. 2020 Aug 3;295(48):16207–16216. doi: 10.1074/jbc.RA120.013899

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© 2020 Smith et al.

Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc.

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Figure 3. — Flux through NNT redox circuits contributes to energy expenditure. A, JO₂ as a function of ΔΨ_m in mitochondria isolated from mouse skeletal muscle during basal respiration supported by PCoA (10 μm), succinate (10 mm), and either low (25 μm) or high (5 mm) carnitine. Note the difference in JO₂ (numbers with arrows) at a given ΔΨ_m (dotted line), indicating difference in proton conductance (i.e. energy expenditure). B, JO₂ measured as a function of ΔΨ_m as described in A in the presence of either low carnitine, high carnitine, or high carnitine plus AF/BCNU (0.1 μm/100 μm). C, JH₂O₂ (left y axis) measured in mitochondria isolated from skeletal muscle of C57BL/6N (+NNT) and C57BL/6NJ (−NNT) mice during respiration supported by PCoA (10 μm) and high (5 mm) carnitine. The percentage of JH₂O₂ buffered (right of dotted line, right y axis) is as defined in Fig. 1B. D, JO₂ measured as a function of ΔΨ_m as described in A in mitochondria isolated from skeletal muscle of C57BL/6N (+NNT) and C57BL/6NJ (−NNT) mice. All data are means ± S.E. (error bars); *, p < 0.05 compared with B6N by unpaired t test; n = 6–12 mice/group.