Single-strand breaks in DNA of hamster and human cells exposed to methyl methanesulfonate and ultraviolet light.
The number of single-strand breaks produced in DNA after exposure to UV light or to methyl methanesulfonate (MMS) was additive when cells were exposed to both agents in close succession. Repair of the damage from either agent was partially inhibited by cytosine arabinoside, resulting in higher break frequencies under all conditions of exposure. Exposure to both agents followed by growth in cytosine arabinoside resulted in break frequencies that were approximately the same as the sum of those from each agent individually. These findings contrast with previous results in which pyrimidine dimer excision and repair replication after exposure to UV light were inhibited by MMS. These observations are not due to cell permeability changes after alkylation, but can be explained if the complex of excision-repair proteins is only partially inactivated by alkylation. Initial incisions to start repair would still occur but only limited amounts of repair replication would ensue without actual removal of the pyrimidine dimers.
D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D006224:Cricetinae; D003412:Cricetulus; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects; D004277:DNA, Single-Stranded; D005260:Female; D005347:Fibroblasts / Q000187:drug effects; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008741:Methyl Methanesulfonate / Q000494:pharmacology*; D010053:Ovary / Q000187:drug effects; D014316:Tritium; D014466:Ultraviolet Rays / Q000009:adverse effects*
D004277:DNA, Single-Stranded; D003561:Cytarabine; D014316:Tritium; D008741:Methyl Methanesulfonate