Mutational damage to human mitochondrial DNA (mtDNA) can cause disorders in oxidative
phosphorylation; speculation that such damage is involved in degenerative diseases and
aging is common. We have detected deletions in mouse mtDNA which resemble those
found in elderly humans or patients with certain mtDNA disorders. Five different mtDNA
deletions, predicted from the positions of short, direct DNA repeats, were present in aged,
but not young, mice. Deleted regions were surrounded by either exact or inexact repeats …