Effects of chronic exposure to ultraviolet B radiation on DNA repair in the dermis and epidermis of the hairless mouse.
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.
Mitchell
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DL
The University of Texas M.D. Anderson Cancer Center, Department of Carcinogenesis, Science Park/Research Division, PO Box 239, Smithville, Texas 78957, USA. dmitch@io.com
Byrom
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M
Chiarello
S
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Lowery
M G
MG
D000818:Animals; D004260:DNA Repair / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D005260:Female; D051379:Mice; D008812:Mice, Hairless; D012867:Skin / Q000528:radiation effects*; D014466:Ultraviolet Rays