Effects of DNA replication inhibitors on UV excision repair in synchronised human cells.
When HeLa cells are irradiated with UV and treated with the DNA synthesis inhibitors hydroxyurea (HU) and 1-beta-D-arabinofuranosylcytosine (ara C), DNA strand breaks accumulate at sites where excision repair of DNA damage has been inhibited after the incision step. This break accumulation occurs in mitotic, G1 and S phase cells. But UV-induced repair synthesis of DNA, as measured by [3H]thymidine incorporation into unreplicated DNA, is not inhibited by HU and ara C in G1 or S phase cells, even though replicative synthesis is virtually abolished. Repair and replication must therefore utilise different DNA precursor pools, or different DNA synthetic systems; and the action of Hu and ara C in causing strand break accumulation may occur at the ligation step of excision repair.
D003561:Cytarabine / Q000494:pharmacology*; D004260:DNA Repair; D004261:DNA Replication / Q000187:drug effects* / Q000528:radiation effects; D006367:HeLa Cells / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology*; D007700:Kinetics; D014466:Ultraviolet Rays
D003561:Cytarabine; D006918:Hydroxyurea