Oxidative Stress, Metabolism and Photoaging – The Role of Mitochondria
The skin is exposed to various endogenous stressors, with solar radiation the most abundant. To modulate cellular dysfunction and repair damage in response to environmental stressors, skin cells are dependent on energy supply. The mitochondria are the primary source of ATP and a decline in mitochondrial function and metabolism is a hallmark of aging, including impairment in mitochondrial morphology, electron transport chain activity, mitochondrial permeability, dynamics and reactive oxygen species formation. Oxidative phosphorylation is the major source of reactive oxygen species underlying mechanism of intrinsic and extrinsic aging. Solar radiation is known to increase oxidative stress in the skin, resulting in damage to mitochondrial protein, structure and mtDNA. Augmented oxidative species levels have been shown to damage biomolecules such as proteins, lipids and nucleic acids, resulting in loss of catalytic activity and/or structural integrity of multiple structures. Decline in mitochondrial efficiency results in elevated reactive species and a free radical vicious cycle hypothesis. Functional decline leads to further decline in energy and insufficient stress response, accelerating the aging process. Understanding the role of mitochondria in the aging pathogenesis is an evolving process. Prevention and alleviation of the oxidative stress, however, remains a paramount strategy in the prevention of cutaneous photoaging.