Cellular hypersensitivity to UV-A: a clue to the aetiology of actinic reticuloid?
Giannelli, F.; Botcherby, P.K.; Marimo, B.; Magnus, I.A.
Lancet 1(8316): 88-91
1983
ISSN/ISBN: 0140-6736 PMID: 6184584 Document Number: 211273
Fibroblasts cultured from 6 patients with actinic reticuloid (AR) showed striking cytopathic changes and inhibition of RNA synthesis after exposure to near-UV radiation that had no effect on normal and other photosensitive cell strains. An abnormal pattern of DNA fragmentation was observed after doses insufficient to cause cytopathic effects. These results suggest a cellular defect in the prevention or repair of some damage caused by free radicals and other photoproducts. In order to explain the pathogenesis of AR, it is proposed that a deficiency in the cellular mechanisms dealing with oxygen radicals leads to the establishment of a vicious circle favoring the persistence of a lymphohistiocytic infiltrate and hence the chronic clinical course characteristic of the disease.