Abstract
Publisher Summary This chapter discusses the role of mitochondrial DNA (mtDNA) modifications in degenerative diseases and aging. The decline in oxidative phosphorylation capacity in degenerative diseases and during aging is related to changes in the mtDNA. It is very likely, albeit not experimentally demonstrated, that the accumulation of modifications in mtDNA is caused to a large extent by oxidation. 8-hydroxydeoxyguanosine (8OHdG), one out of many oxidatively generated modified bases, is formed in DNA by reactive oxygen species (ROS) in vitro, is present in high amounts in mtDNA, and is an established mutagen. ROS also cause strand breaks in mtDNA in vitro. Therefore, it is reasonable to assume that ROS may be the agents responsible for many of the observed base modifications and fragmentation of mtDNA in vivo. Experimental tests of this assumption are possible. An understanding of the role of mtDNA mutations in diseases suggests an improved diagnosis at the molecular level. Both point mutations and deletions in mtDNA can be analyzed in DNA taken from blood samples.
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