UV radiation (UVR) produces
erythema within the first 24 hours of exposure, suppression of the immune system within the first 10 days, and, for many people, over the course of decades,
skin cancer. Although UVR damages many skin targets, DNA damage in the form of
cyclobutane pyrimidine dimers (CPDs) is an important mediator of these sequelae. The action spectrum for
erythema parallels the action spectrum for CPD formation in skin, and in the absence of repair, as in the
genetic disease xeroderma pigmentosum (XP),
skin cancer rates are dramatically increased. DNA repair in skin can be enhanced by the delivery of
DNA repair enzymes encapsulated in
liposomes. Used in this way, photoreactivation of CPDs greatly diminishes
erythema and the suppression of
contact hypersensitivity (CHS). UV
endonucleases delivered by
liposomes also prevent UV-induced suppression of delayed-type
hypersensitivity. In a clinical study of patients with XP,
T4 endonuclease V (T4N5)
liposome lotion applied for one year reduced the rates of
actinic keratosis (AK) and
skin cancer compared with placebo. These results showed that strategies to increase sun protection should include measures to reduce DNA damage and increase the rate of DNA repair.