Differential photoimmunoprotection by sunscreen ingredients is unrelated to epidermal cis urocanic acid formation in hairless mice

Abstract

A series of experimental sunscreen preparations based on a common vehicle, containing increasing concentrations of either octyl-N-dimethyl-p-aminobenzoate (o-PABA) or 2-ethylhexyl-p-methoxycinnamate (2-EHMC) as the ultraviolet B (UVB) absorber, has been tested in the hairless mouse for the ability to protect from erythema, from the systemically suppressive effects of UVB (280-320 nm) radiation on contact hypersensitivity, and from photoisomerization of epidermal urocanic acid. All the preparations protected efficiently from the edema component of the erythema response when mice were exposed to UVB radiation equivalent to three times the minimal erythema dose (MED). However, when mice were exposed to UVB radiation equivalent to 15 x MED, protection from erythema was observed only at the higher concentrations of each UVB absorber (10% 2-EHMC and 10% or 15% o-PABA). Protection from the UVB-induced suppression of contact hypersensitivity was shown to be dependent on both the nature of the UVB absorber and its concentration. Photoimmunoprotection by the sunscreens containing 2-EHMC was evident at lower concentrations (5% and 10% 2-EHMC) than with o-PABA, following both 3 x MED and 15 x MED of UVB exposure. Photoimmunoprotection by o-PABA-containing sunscreens was observed only at 15% o-PABA following 3 x MED, and failed at all tested concentrations after 15 x MED of UVB exposure. Regardless of the photoimmunoprotective capacity, sunscreen preparations containing either of the UVB absorbers prevented the UVB-induced formation of cis urocanic acid in the mouse epidermis and in vitro under all conditions tested. Thus, there appeared to be a correlation between protection from edema and from cis urocanic acid formation at 3 x MED of UVB, but a dissociation of these variables at 15 x MED of UVB. There was no relation apparent at either UVB dose between either edema or cis urocanic acid formation and protection from suppression of contact hypersensitivity.