Figure 2.

Increased mtDNA damage, mitochondrial (M) respiration function, and intracellular free radical production in mMT-hOGG1 TG mice. A: Decreased mtDNA copy numbers in the liver, kidney, brain, and skeletal muscle from mMT-hOGG1 TG mice compared with those from wild-type control mice (CO). The bars indicate the mean ± SE (n = 4 for liver and kidney; n = 5 for skeletal muscle; n = 6 for brain). B: Increased mtDNA deletions in hOGG1 TG mice compared with those in CO. The mtDNA deletions (Del) (3729, 12,622, and 15,139 bp) and corresponding wild-type (WT) mtDNA were analyzed in liver (lanes 1 and 5), brain (lanes 2 and 6), skeletal muscle (lanes 3 and 7), and brown fat (lanes 4 and 8) tissues from hOGG1 TG (lanes 1 to 4) and WT (lanes 5 to 8) control mice. C: Increased mitochondrial ND1 mRNA, indicating increased mitochondrial respiratory function, in liver and kidney tissues from hOGG1 TG mice compared with those from CO. The bars indicate the mean ± SE (n = 4 for control mice; n = 7 for TG mice). D: Increased production of H₂O₂ in liver and kidney tissues of mMT-hOGG1 TG mice compared with that of CO. The bars indicate the mean ± SE (n = 5).