ULTRAVIOLET-LIGHT AND FREE-RADICALS - AN IMMUNOLOGICAL THEORY OF EPIDERMAL CARCINOGENESIS

Ultraviolet light (UV) damages lipids, proteins, and DNA. Lipid peroxides combine with proteins to form Schiff bases, proteins cross-link, and nucleotides generate thymine dimers. The major epidermal cell population, keratinocytes, undergoes a distinct form of cell death, termed apoptosis, which may be a genetically programmed attempt to remove neoplastic cell clones. Lan- gerhans’ cells, the “macrophages” of the epidermis, are responsible for removing the surviving neoplastic clones. UV light, however, reduces their ability to present antigens to T-cell lymphocytes and to remove cells that have escaped apoptosis. The surviving neoplastic cells can grow unchecked, giving rise to frank neoplasia. Traditional sunscreens, para-aminobenzoic acid and sulisoben- zone, may still allow low doses of U V radiation to down- regulate the immune system. Three agents hold promise in preventing epidermal immunologic alterations: retinoids, polyamines, and antioxidants. Retinoids and polyamines may increase epidermal thickness, protect radiosensitive basal layers, and promote differentiation. Antioxidants (vitamins C and E) may limit damage by terminating UV-induced free-radical chain reactions. Research is needed to determine the value of these agents individually and in combination in the hopes of developing a true sunscreen. © 1990 American Society of Plastic Surgeons.