The mechanism of N-acetylcysteine photoprotection is not related to dipyrimidine photoproducts

Topical application of N-acetylcysteine prior to UVB irradiation of BALB/c mice has previously been shown to inhibit systemic suppression of the contact hypersensitivity response. Formation of cis-urocanic acid, however, is not affected. Besides urocanic acid, UV-induced DNA damage has been held responsible for the initiation of suppression of the contact hypersensitivity response. Therefore, the possible inhibitory effect of N-acetylcysteine on UVB-induced cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts has been investigated. No effect on the photoproducts studied is observed, suggesting that N-acetylcysteine exerts its photoprotective effect during the post-initiation phase of photoimmunosuppression.