Byfield J E, Lee Y C, Tu L, Kulhanian F
Cancer Res. 1976 Mar;36(3):1138-43.
The interactions between bleomycin and X-ray damage and repair have been examined in rat and human tumor cells. Bleomycin itself indices extensive DNA single-strand breaks but does not appear to inhibit the repair of X-ray-induced DNA single-strand breaks. Quantitative analysis of these interactions is complicated by the retention of active bleomycin within cells that remains capable of further DNA degradation even under the conditions of alkaline sucrose gradient cell lysis. DNA double-strand breaks and/or disruptions of DNA-lipid complexes also occur following bleomycin exposure. X-ray-induced excision repair replication is only minimally influenced by even high concentrations of bleomycin. A small amount of excision repair is demonstrable in nonirradiated cells treated with high concentrations of bleomycin consistent with repair of bleomycin-induced nucleotide damage in cellular DNA by a "cut and patch" repair mechanism. Repair of bleomycin-induced DNA single-strand breaks also occurs. The data indicate that bleomycin and X-ray damage are quite similar both in their induction and repair, but that lesions occur and are repaired independently. The enzymatic mechanisms appear similar in the two cell types despite substantial differences in their sensitivity to bleomycin.
已经在大鼠和人类肿瘤细胞中研究了博来霉素与X射线损伤及修复之间的相互作用。博来霉素本身会导致广泛的DNA单链断裂，但似乎并不抑制X射线诱导的DNA单链断裂的修复。这些相互作用的定量分析因细胞内活性博来霉素的保留而变得复杂，即使在碱性蔗糖梯度细胞裂解的条件下，这些保留的博来霉素仍能够进一步降解DNA。博来霉素暴露后也会发生DNA双链断裂和/或DNA-脂质复合物的破坏。即使是高浓度的博来霉素对X射线诱导的切除修复复制的影响也很小。在用高浓度博来霉素处理的未受辐射的细胞中可证明有少量的切除修复，这与通过“切割和修补”修复机制修复细胞DNA中博来霉素诱导的核苷酸损伤一致。博来霉素诱导的DNA单链断裂也会发生修复。数据表明，博来霉素和X射线损伤在诱导和修复方面非常相似，但损伤是独立发生和修复的。尽管两种细胞类型对博来霉素的敏感性存在很大差异，但酶促机制似乎相似。
