Ultraviolet Light and Free Radicals

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Abstract
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. Langerhans' 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 sulisobenzone, may still allow low doses of UV 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.
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