Research Paper Volume 1, Issue 3 pp 303—315

Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice

Figure 2. (A) Mitochondrial respiration of muscle fibers. 10 to 25 mg of permeabilized bundles were analyzed by high resolution respirometry. Results are expressed as oxygen consumption per mg of muscle (± SEM) normalized to citrate synthase activity of n=5 to 6 mice per group. State III respiration is shown after addition of malate, octanoyl-carnitine, ADP, glutamate, succinate and cytochrome c. After state III respiration determination, uncoupled respiration was determined with addition of FCCP to the respiring fibers. Rotenone and antimycin A were used to inhibit respiration at complex I and III respectively. (B) Oxidative modifications (fpg sites) in DNA from bone marrow cells of 12 to 17 month old mice. Data from n=4 to 9 mice per group is shown as number of lesions per 106 bp ± SEM. (C) Representative pictures of gH2AX staining in intestinal crypts of aged mice and bar graphs (D) showing percentage of positive cells per crypt and number of foci per cell ± SEM of n=4 to 6 mice per group. 200 crypt cells were analyzed per mouse. (E) Telomere length analysis by qFISH in liver sections of n= 4 to 5 mice per group aged 12 to 18 months old. n=237 G3 mTerc-/-, Sod2+/-), n=234 (G3 mTerc-/-, Sod2+/+); n=242 (mTerc+, Sod2+/-) and n=211 (mTerc+, Sod2+/+) nuclei were analyzed for telomere fluorescence intensity (TFI). The black line indicates the mean TFI value of each genotype and the dotted line the threshold of critically short telomeres (TFI<3500).