INTRODUCTION
Skin exposure to ultraviolet radiation (UVR) causes DNA damage, which can lead to mutagenesis, carcinogenesis, cellular death, and photoaging. The term photoaging refers to the premature aging of skin that results from chronic exposure to UVR. Histopathologically, photoaged skin shows a decreased collagen content, decreased elastin and disintegration of elastin fibers, and a reduced density of cutaneous microvasculature, among other microscopic changes.1 Clinical signs of photoaging include wrinkling, erythema, skin laxity, uneven skin texture, and hyperpigmentation. Although endogenous DNA repair mechanisms exist, some damage persists and can accumulate with continued UV exposure leading to permanent damage to the skin structure.
Photolyase is a naturally occurring DNA repair enzyme that uses a light-dependent process to restore DNA integrity but is absent in humans and other placental mammals. Numerous in vitro and clinical studies over the past several decades have supported the addition of exogenous photolyase to topical preparations to augment human DNA repair mechanisms, allowing for more efficient prevention and repair of UVR damage.2 This function has been demonstrated through the reversal of cyclobutane pyrimidine dimers (CPDs),3-6 prevention of apoptotic cell death,5 as well as the treatment of mild to moderate actinic keratoses.7 Photolyase has also been shown to defend against photoaging through multiple mechanisms including the reduction of pro-inflammatory cytokine IL-64 and
Photolyase is a naturally occurring DNA repair enzyme that uses a light-dependent process to restore DNA integrity but is absent in humans and other placental mammals. Numerous in vitro and clinical studies over the past several decades have supported the addition of exogenous photolyase to topical preparations to augment human DNA repair mechanisms, allowing for more efficient prevention and repair of UVR damage.2 This function has been demonstrated through the reversal of cyclobutane pyrimidine dimers (CPDs),3-6 prevention of apoptotic cell death,5 as well as the treatment of mild to moderate actinic keratoses.7 Photolyase has also been shown to defend against photoaging through multiple mechanisms including the reduction of pro-inflammatory cytokine IL-64 and