DNA damage induced by nitric oxide during ionizing radiation is enhanced at replication

摘要: Abstract Nitric oxide ( NO) is a very effective radiosensitizer of hypoxic mammalian cells, at least as efficient oxygen in enhancing cell death vitro. NO may induce through the formation base lesions which are difficult to repair, and if they occur within complex clustered damage common ionizing radiation, lead replication-induced DNA strand breaks. It has previously been shown that 8-azaguanine xanthine result from reaction guanine radicals with nitric oxide. We have now adenine also react form hypoxanthine 8-azaadenine. Cells irradiated exponential growth presence twice radiosensitive compared those anoxia alone, whereas confluent cells less •NO. In addition, numbers double breaks observed γH2AX staining following radiosensitization by NO, higher than cells. damage, detected 53BP1 foci, HF-19 expressing Cyclin A, marker for S G2 phases cycle, NO. RAD51 foci highest V79-4 anoxia, 24 h after radiolysis. This work presents evidence part specific dividing stalled replication forks consequence death.