Research Paper Volume 9, Issue 2 pp 315—339

Improved health-span and lifespan in mtDNA mutator mice treated with the mitochondrially targeted antioxidant SkQ1

Figure 7. Effect of SkQ1 treatment on function of isolated mitochondria. (A) Example of an oxygen consumption trace in mitochondria isolated from skeletal muscle of mtDNA mutator mouse. Additions were 0.25 mg skeletal muscle mitochondria (SKM), 5 mM pyruvate (Pyr), 250 µM ADP, 2 µg /ml oligomycin (Olig) and 1.4 µM FCCP. (B) Rates of oxygen consumption in mitochondria isolated from skeletal muscle of SkQ1-treated and non-treated mtDNA mutator mice. Analysis was performed as shown in 7A. (C) Amplex Red fluorescence in intact mitochondria isolated from skeletal muscle of mtDNA mutator mouse. Additions were 0.25 mg skeletal muscle mitochondria (SKM), 5 mM pyruvate (Pyr), 5mM succinate (Succ). Malate (3 mM) was present in the medium. The analyses were performed in the same mitochondrial preparations as in (A) in parallel with the oxygen consumption measurements. (D) Rates of hydrogen peroxide production in mitochondria isolated from skeletal muscle of wild type mice (WT), SkQ1 non-treated (Mut) and treated (Mut + SkQ1) mtDNA mutator mice. Analysis was performed as shown in C. P+M indicates the presence of complex I substrates (pyruvate + malate) and P+M+S indicates the presence of three substrates (pyruvate + malate + succinate). In A and D, the values represent the means ± S.E. of 6 independent mitochondrial preparations isolated in parallel from treated and non-treated groups of mice of an age of 252 – 259 days. * in A-D indicates statistical difference between SkQ1-treated and non-treated mice (p < 0.05).