INTRODUCTION
Deoxynucleic acid (DNA) damage caused by ultraviolet (UV) light in humans has been well documented and described in the literature.1-5 However, the ability to detect DNA damage is typically only confirmed after gross morphological evidence exists, as seen in precancerous and cancerous lesions on the skin.
The ability to treat DNA damage and restore skin to the original state before it is grossly damaged remains a clinical challenge. There are intrinsic mechanisms known to repair DNA damage in bacteria, plants, and some animals, but humans seem to have limited options for this process and are thought to rely mainly on nucleotide excision repair (NER) mechanisms.6-8 Moreover, there is evidence that impaired DNA repair may be a susceptibility factor for sunlight-induced skin cancer in the general population.9 The use of topical DNA repair enzymes, specifically T4 Endonuclease V (T4N5) and photolyases, have previously demonstrated the ability to assist in the removal of cyclobutane pyrimidine dimers formed after UV irradiation.10-12 These DNA repair enzymes have also been proven to reduce skin cancer and precancerous skin lesions, namely actinic keratoses.13,14 Wolf et al demonstrated that application of T4N5 after UV exposure nearly completely prevented the upregulation of interleukin-10 and tumor necrosis factor alpha (TNFα), cytokines that are normally upregulated in UV-induced immune suppression.15 In addition, a cousin DNA repair enzyme derived from Micrococcus luteus (M. luteus), has shown promise in the prevention of actinic keratoses and skin cancers.16-19
The innovation of non-invasive, adhesive skin collection kits (DermTech, Inc., La Jolla, CA) may allow for the early detection of DNA damage in human skin cells at the molecular level after acute and/or chronic exposure to ultraviolet light. This new technology may also have the ability to monitor the recovery
The ability to treat DNA damage and restore skin to the original state before it is grossly damaged remains a clinical challenge. There are intrinsic mechanisms known to repair DNA damage in bacteria, plants, and some animals, but humans seem to have limited options for this process and are thought to rely mainly on nucleotide excision repair (NER) mechanisms.6-8 Moreover, there is evidence that impaired DNA repair may be a susceptibility factor for sunlight-induced skin cancer in the general population.9 The use of topical DNA repair enzymes, specifically T4 Endonuclease V (T4N5) and photolyases, have previously demonstrated the ability to assist in the removal of cyclobutane pyrimidine dimers formed after UV irradiation.10-12 These DNA repair enzymes have also been proven to reduce skin cancer and precancerous skin lesions, namely actinic keratoses.13,14 Wolf et al demonstrated that application of T4N5 after UV exposure nearly completely prevented the upregulation of interleukin-10 and tumor necrosis factor alpha (TNFα), cytokines that are normally upregulated in UV-induced immune suppression.15 In addition, a cousin DNA repair enzyme derived from Micrococcus luteus (M. luteus), has shown promise in the prevention of actinic keratoses and skin cancers.16-19
The innovation of non-invasive, adhesive skin collection kits (DermTech, Inc., La Jolla, CA) may allow for the early detection of DNA damage in human skin cells at the molecular level after acute and/or chronic exposure to ultraviolet light. This new technology may also have the ability to monitor the recovery
