DNA repair in normal human and xeroderma pigmentosum group A fibroblasts following treatment with various methanesulfonates and the demonstration of a long-patch (u.v.-like) repair component.
Excision repair of DNA in normal and xeroderma pigmentosum complementation group A fibroblasts were examined following treatment with methyl-, ethyl-, and isopropyl methanesulfonate. Studies utilizing repair synthesis methods and inhibition with arabinofuranosyl cytosine revealed two distinct phases of repair; one commencing and terminating within the first 3-5 h after the treatment, and a second much longer phase extending from 9-35 h post-treatment. Both phases of repair have a long-patch (u.v.-like) component, which establishes for the first time the existence of this mode of repair in response to alkane sulfonate damage. While xeroderma cells display somewhat fewer alkaline labile sites in their DNA following alkylation treatment than do their normal counterparts (consistent with earlier observations suggesting a deficiency in a glycosylase or apurinic endonuclease), we are unable to demonstrate a deficiency of these cells in either of the two phases of repair.
D000477:Alkylating Agents / Q000633:toxicity; D000478:Alkylation; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects*; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D008698:Mesylates / Q000633:toxicity*; D010782:Photolysis; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000235:genetics / Q000378:metabolism*
D000477:Alkylating Agents; D008698:Mesylates; D003561:Cytarabine