Photoaging-associated large-scale deletions of mitochondrial DNA

Heteroplasmy, replicative segregation, low copy numbers of mtDNA, and selection mechanisms at the molecular and cellular level are all factors that determine requirements toward the experimental design for the detection and the quantification of mtDNA mutations. The short half-life and low stability of ROS further increase the technical demands. However, the continuous improvement of techniques has given us more insight into the interactions between ROS and mtDNA, both at the level of endogenous ROS produced by the normal mitochondrial metabolism and exogenous sources of ROS, such as singlet oxygen, which can result from treatments such as UVA exposure.