Additionally, oxidative damage to mitochondrial DNA (mtDNA) has been described to play a major role in photoaging (3). Studies have shown that a common deletion of mtDNA is increased about 10-fold in photoaged skin as compared to sun-protected skin in the same individual (4). Although normal ATP production in the mitochondria results in some level of oxidative stress, it is thought that UVA exposure increases oxidative stress in the mitochondria what leads to mutations of mtDNA and consequently to a defective respiratory chain. The defective respiratory chain results in reduced energy production by the mitochondria and increased production of ROS (5-8). This increase in ROS leads to more mtDNA mutations which further perpetuate the production of ROS. As a consequence, mtDNA mutations will increase even in the absence of UV exposure (3,9). This hypothesis has been termed “the defective powerhouse model of premature skin aging” (3).