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.
Nijmeijer
B A
BA
Department of Medicinal Photochemistry, Leiden/Amsterdam Center for Drug Research, Netherlands.
Steenvoorden
D P
DP
Beijersbergen van Henegouwen
G M
GM
Roza
L
L
Vink
A A
AA
D000111:Acetylcysteine / Q000378:metabolism*; D000818:Animals; D004249:DNA Damage / Q000528:radiation effects; D004817:Epidermis / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011743:Pyrimidines / Q000378:metabolism*; D014466:Ultraviolet Rays
D011743:Pyrimidines; D005978:Glutathione; D000111:Acetylcysteine