| Literature DB >> 11179995 |
D L Mitchell1, M Byrom, S Chiarello, M G Lowery.
Abstract
It has previously been shown that chronic exposure to low fluences of ultraviolet B radiation reduced DNA repair capacity in mouse skin. In this study we now extend this to examine the concentration dependence and tissue dependence of this phenomenon. We found that (6-4) photoproducts were repaired considerably faster than cyclobutane dimers and that the kinetics for photoproduct removal were comparable in the dermis and epidermis. Chronic ultraviolet B irradiation significantly reduced the initial rate and extent of DNA repair. After low daily doses of ultraviolet B (6-4) photoproduct repair was most affected and after high daily doses the repair of both cyclobutane and (6-4) dimers was reduced. Whereas cyclobutane dimer repair was most affected in the dermis, reduced (6-4) photoproduct repair was observed in both tissues. The deleterious effects of chronic ultraviolet exposure were sustained for a considerable time after the chronic treatment ended.Entities:
Mesh:
Year: 2001 PMID: 11179995 DOI: 10.1046/j.1523-1747.2001.01192.x
Source DB: PubMed Journal: J Invest Dermatol ISSN: 0022-202X Impact factor: 8.551