Pyrimidine dimer induction and removal in the epidermis of hairless mice: inefficient repair in the genome overall and rapid repair in the H-ras sequence.
Excision repair of pyrimidine dimers was examined at the genome overall in three strains of hairless (hr/hr) and congenic wild-type mice, as well as in the expressed H-ras gene in hairless mice. The assay used a pyrimidine dimer-specific endonuclease from Micrococcus luteus and alkaline agarose gel electrophoresis. From 0 to 25% of endonuclease-sensitive sites were removed at the genome level in either hairy or hairless mice but about 50% were removed in the H-ras gene in hairless mice by 24 h after exposure to 5.4 J/cm2 UV (290-400 nm) irradiation. No differences were observed in the repair capacity between hairy and hairless mice, thus eliminating defective DNA repair as the explanation for the greater susceptibility to UV carcinogenesis in hairless mice.
Department of Animal Science, University of Sydney, NSW, Australia.
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Greenoak
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Moran
D000818:Animals; D004260:DNA Repair / Q000235:genetics*; D005260:Female; D011905:Genes, ras; D051379:Mice; D008812:Mice, Hairless; D008807:Mice, Inbred BALB C; D011740:Pyrimidine Dimers / Q000378:metabolism / Q000528:radiation effects*; D012867:Skin / Q000378:metabolism / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects
D011740:Pyrimidine Dimers