EFFECTS OF SUNSCREENS AND A DNA EXCISION-REPAIR ENZYME ON ULTRAVIOLETRADIATION-INDUCED INFLAMMATION, IMMUNE SUPPRESSION, AND CYCLOBUTANE PYRIMIDINE DIMER FORMATION IN MICE

Exposure of skin to ultraviolet (UV) radiation inhibits the induction of delayed-type hypersensitivity (DTH) responses initiated at a distan t, unirradiated site. Recent studies attributed this form of immune su ppression to DNA damage in the form of cyclobutane pyrimidine dimers ( CPD). In the present study, we investigated the protective defects of sunscreens on UV-induced systemic suppression of DTH to Candida albica ns, inflammation, and DNA damage. The photoprotective effects of sunsc reen preparations containing 8% octyl-N-dimethyl-p-aminobenzoate, 7.5% 2-ethylhexyl-p-methoxycinnamate, or 6% benzophenone-3 were studied in C3H mice exposed to a single dose of 500 mJ/cm2 UVB radiation from FS 40 sunlamps. Inflammation was determined by the amount of skin edema a t the site of UV irradiation, and DNA damage was assessed by measuring the frequency of endonuclease-sensitive sites in the epidermis. Appli cation of the sunscreens before UV irradiation gave 75-97% protection against UV-induced edema, 67-91% Protection against formation of CPD, but only 30-54% protection against suppression of DTH. In contrast, th e topical application of liposomes containing a CPD-specific DNA repai r enzyme immediately after UV irradiation resulted in 82% protection a gainst suppression of DTH, but at best, 39% protection against skin ed ema. These findings demonstrate that sunscreens give less protection a gainst UV-induced immune suppression than against skin edema and CPD f ormation. Furthermore, they suggest that less DNA damage is required t o cause UV-induced immune suppression than to cause sunburn.