Accumulated damage to mitochondrial DNA is an important component of aging. Mitochondria are the cell's powerplants, and their DNA, separate from that contained in the cell nucleus, is vulnerable to the reactive by-products of mitochondrial operation. Intricate DNA repair processes exist, but eventually they become outmatched, and broken mitochondria dominate in a small but significant fraction of our cells. These cells become very active exporters of harmful, reactive biochemicals, which in turn causes progressively greater damage to biological processes throughout the body - and in the fullness of time this helps to kill you.
What we would like to see happen in the near future is for any one of the several lines of research into mitochondrial repair to advance to completion. Whole body repair of mitochondrial DNA damage conducted once every two or three decades would eradicate this important contribution to degenerative aging.
In the meanwhile, here's an open access paper that looks more closely at mitochondrial damage over time in the eyes, a process that contributes to the formation of catacts:
Oxidative damage resulting from reactive oxygen species (ROS) is considered to be a major risk factor in the pathogenesis of both age-related and diabetic cataract. ROS is mostly generated within the mitochondria in lens epithelium and the superficial fiber cells, which are highly reactive and can damage macromolecules in living cells, [causing] mutagenesis and cell death. Mitochondrial DNA (mtDNA) is highly susceptible to the damage produced by ROS because of its close proximity to ROS generation through the respiratory chain.
The 'mitochondrial theory of aging' suggests that aging results from declining mitochondrial function, due to high loads of damage and mutation in mtDNA. Oxidative damage to mtDNA has been implicated as a causative factor in a wide variety of degenerative diseases, in cancer, and in aging . Under normal growth conditions, ROS leads to a low level of mtDNA and nuclear DNA (nDNA) damage, which is rapidly repaired, and most oxidative DNA lesions are repaired by the base excision repair (BER) pathway
The purpose of the study presented here was to determine if there is an increased mtDNA [damage] in the lens with age.
The gene expression [of] key BER enzymes decreased with age, which caused a decrease in the repairing capability of the mtDNA and the accumulation of mtDNA damage. The increased mtDNA damage and decreased expression of BER enzymes may cause a "vicious cycle" of oxidative stress that contributes to the accumulation of mtDNA mutations and age-related cataract pathogenesis.
As hinted at here, the growth of mitochondrial damage, like most aspects of biology, is a very dynamic process. Human biology strives to maintain itself, and most of its self-repair systems are very effective indeed - in the young, at least. Aging is as much a progressive failure of biological repair mechanisms as it is an accumulation of damaged and misplaced machinery.