Research Paper Volume 1, Issue 3 pp 303—315

Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice

Figure 1. Western blots showing SOD2 levels in liver (A), brain (B) and bone marrow (C) of 12 to 18 months old mice. Lower panels show representative western blots and upper panels show quantification of normalized SOD2 levels to actin controls from n=4 mice per group (1 to 2 repeat experiments per sample). Data is shown in arbitrary units ± SEM. (D) Basal ROS levels in muscle fibers stained with DHE. Signal quantification of G3 mTerc-/-Sod2+/- (n=235), G3 mTerc-/-(n=211) mTerc+, Sod2+/-(n=270 ) and mTerc+, Sod2+/+ (n=203) nuclei from 5 mice per genotype. Data is shown as mean fluorescence intensity ± SEM. (E) Antioxidant capacity of LSK cells. DCFDA loaded bone marrow cells were incubated with 50 uM of antimycinA and DCFDA fluorescence was monitored in Lin-Sca+cKit+ populations by FACS analysis. Data is shown in arbitrary units ± SEM of n=4 mice per group. (F) Antioxidant capacity of myeloid cells. Mitosox loaded bone marrow cells were incubated with 20 uM antimycinA and mitosox intensity monitored in myeloid population by FACS analysis. "Y" axis denotes arbitrary units for fluorescence intensity of n=5 to 6 mice per group.