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Fig. 1 | Skeletal Muscle

Fig. 1

From: RETRACTED ARTICLE:Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice

Fig. 1

Endurance exercise reduces random mtDNA somatic mutations, attenuates mitochondrial ROS-mediated oxidative damage, mitigates telomere shortening, and reduces nuclear accumulation of p53 in mtDNA mutator mice. a Random mtDNA somatic mutation rate (per 1000 nucleotides of mtDNA) in muscle (quadriceps femoris) WT, PolG-SED, and PolG-END mice (n = 4–5/group). b H2O2 production rate in muscle mitochondrial fractions of WT, PolG-SED, and PolG-END (n = 5–7/group). Complex I and II substrates: P/M, pyruvate/malate and SUC, succinate (5 mM each), respectively. Complex I and III inhibitors: ROT, rotenone, and AA, antimycin A (0.5 μM each), respectively. c Protein carbonyls (PC) content in muscle (tibialis anterior) and heart mitochondrial fractions of WT, PolG-SED, and PolG-END (n = 5–7/group). d SOD2 and catalase enzyme activity in the muscle (quadriceps femoris) and heart of WT, PolG-SED, and PolG-END (n = 7/group). e Average telomere length ratios in the heart, hematopoietic stem and progenitor cells (HSC), and satellite cells (SC) of WT, PolG-SED, and PolG-END (n = 6–8/group). f Representative blots of nuclear p53 content (~53 kDa) in the muscle (quadriceps femoris) and heart of WT, PolG-SED, and PolG-END (n = 5–8/group). Histone H2B (~14 kDa) was used as a nuclear loading control. (PolG-SED vs. both WT and PolG-END) = *P < 0.05, **P < 0.01; (PolG-END vs. WT) =  P < 0.05. Error bars represent SEM. AU arbitrary units

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