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. Author manuscript; available in PMC: 2010 Jun 2.
Published in final edited form as: Circulation. 2009 May 18;119(21):2789–2797. doi: 10.1161/CIRCULATIONAHA.108.822403

Figure 3. Mitochondrial DNA mutations, oxidative damage and biogenesis in aged heart and the protective effect of mCAT.

Figure 3

A) Mitochondrial DNA point mutation and B) deletion frequencies (both per million) increased significantly with age and were better preserved in OmCAT mouse hearts. C) Mitochondrial protein carbonyls (nmol/mg) increased significantly in old age, while OmCAT mice were better protected from oxidative damage to mitochondrial proteins. D) Mitochondrial DNA copy number (normalized to young WT) increased significantly with age, and old mCAT mice had significantly lower mitochondrial DNA copy number. E). Genes involved in mitochondrial biogenesis, PGC-1α, TFAM, NRF-1 and NRF-2, were upregulated in aged heart, and changes in PGC-1α and TFAM were attenuated in old mCAT mice (*p<0.025 between young vs. old WT, #p<0.025 between old WT vs. mCAT; n=9-12 each group; old: 26-28 months, young:4-5 months old).