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Induction and repairability of DNA damage caused by ultrasoft X-rays: role of core events.

机译:超软X射线引起的DNA损伤的诱导和可修复性:核心事件的作用。

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摘要

PURPOSE: To investigate the severity of damage induced in plasmid DNA by ultrasoft X-rays at different energies, in order to unravel the correlation between the sharp increase in cell-killing efficiency of ultrasoft X-rays above versus below the carbon K-threshold and the induction of core events in DNA atoms. MATERIALS AND METHODS: Bluescript (pBS, tight packing) and pSP189 (pSP, loose packing) plasmids were exposed to ultrasoft X-rays at 250, 380 and 760 eV energies, respectively, above phosphorus L-, carbon K- and oxygen K-thresholds. Complex DNA lesions were assayed by the repair protein Formamidopyrimidine DNA glycosylase (Fpg) and by in vitro repair assay using whole cell-free extracts. RESULTS: Clustered damage, as revealed by Fpg-induced double strand breaks, was observed at low level, but at similar rate at the three energies. Damage induced at 380 eV may be slightly less efficiently repaired by cell extracts than those produced at 250 eV. 760 eV photons which yield longer range electrons than250 and 380 eV photons, induced more total damages which were more efficiently repaired, and thus likely more dispersed. CONCLUSION: It is demonstrated that ultrasoft X-rays induce complex damage, which do not exhibit the same ability to be repaired, depending on the energy and on DNA packing.
机译:目的:研究超软X射线在不同能量下对质粒DNA造成的损伤的严重程度,以揭示碳K阈值以上和以下碳源的超软X射线对细胞杀伤效率的急剧增加与降低之间的相关性。 DNA原子中核心事件的诱导。材料与方法:将Bluescript(pBS,紧密堆积)和pSP189(pSP,疏松堆积)质粒分别以250、380和760 eV能量分别暴露于磷L-,碳K-和氧K-以上的超软X射线阈值。复杂的DNA损伤可通过修复蛋白Formamidopyrimidine DNA糖基化酶(Fpg)进行测定,并使用无细胞全提取物进行体外修复测定。结果:Fpg诱导的双链断裂显示出簇状损伤,在低水平观察到,但在三种能量下以相似的速率观察到。与在250 eV产生的损伤相比,细胞提取物修复在380 eV诱导的损伤的效率可能略低。 760 eV光子产生的远距离电子比250和380 eV光子更长,产生了更多的总损伤,这些损伤可以得到更有效的修复,因此可能更分散。结论:证明了超软X射线会引起复杂的损伤,根据能量和DNA的堆积情况,它们不会表现出相同的修复能力。

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