Research Paper Volume 4, Issue 1 pp 3—12
Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin
Figure 2. Sod2 expression and mitochondrial activity in skin of WT and Sod2−/− mice.
(A) Western analysis for SOD2 and α-tubulin (αTUB) in dorsal skin samples from WT (n=6) and Sod2−/− (n=6) mice, aged 17-20 days. (B) Quantitative PCR analysis of Sod2 mRNA levels in skin of WT (n=8) and Sod2−/− (n=9) mice. Transcript levels were normalized to beta-actin levels. Means with asterisks indicate significant differences at p<0.05 by Student's t test. (C, D) Representative photo-micrographs of skin sections from WT (n=8) and Sod2−/− (n=9) mice, aged 17-20 days, stained for succinate dehydrogenase (SDH) (C; blue) and cytochrome c oxidase (COX) (D; brown) activities.