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V79-4 仓鼠细胞中双链断裂的诱导与修复:应用超软 X 射线探测的核心离化作用。

Double-strand break induction and repair in V79-4 hamster cells: the role of core ionisations, as probed by ultrasoft X-rays.

机构信息

Institut de Minéralogie et de Physique des Milieux Condensés, Université Pierre et Marie Curie-Paris6, UMR-CNRS 7590, Paris, France.

出版信息

Int J Radiat Biol. 2010 Mar;86(3):205-19. doi: 10.3109/09553000903419296.

Abstract

PURPOSE

To compare the induction of double-strand breaks (DSB) in cells irradiated by 250 and 350 eV ultrasoft X-rays and assess the residual yield of breaks 2 hours post irradiation 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 (284 eV) and the induction of core events in DNA atoms.

MATERIALS AND METHODS

V79-4 hamster cells were irradiated with synchrotron ultrasoft X-rays at isoattenuating energies of 250 eV and 350 eV. DSB were quantified using pulse field gel electrophoresis.

RESULTS

A significant increase in DSB induction was observed for 350 eV ultrasoft X-rays above the carbon-K threshold, compared to 250 eV below the threshold, per unit dose to the cell. The DSB induced by the 350 eV ultrasoft X-rays were less repaired 2 h after irradiation.

CONCLUSION

The increased DSB induction at 350 eV is attributed to the increase in the relative proportion of photon interactions in DNA resulting in significant dose inhomogeneity across the cell with a local increase in dose to DNA. It results from an increase in carbon-K shell interactions and the short range of the electrons produced. Core ionisations in DNA, through core-hole relaxation in conjunction with localised effects of spatially correlated low-energy photo- and Auger-electrons lead to an increase in number and the complexity of DSB.

摘要

目的

比较 250 和 350 eV 极软 X 射线照射细胞时诱导双链断裂(DSB)的情况,并评估照射后 2 小时断裂的剩余产量,以揭示极软 X 射线在碳 K 阈值(284 eV)以上和以下时细胞杀伤效率的急剧增加与 DNA 原子中核心事件的诱导之间的相关性。

材料和方法

用同步加速器极软 X 射线以等衰减能量 250 eV 和 350 eV 照射 V79-4 仓鼠细胞。使用脉冲场凝胶电泳定量 DSB。

结果

与低于阈值的 250 eV 相比,在碳 K 阈值以上的 350 eV 极软 X 射线中,单位细胞剂量下 DSB 的诱导显著增加。与照射后 2 小时相比,350 eV 极软 X 射线诱导的 DSB 修复较少。

结论

350 eV 时 DSB 诱导的增加归因于光子相互作用在 DNA 中相对比例的增加,导致细胞内剂量不均匀,DNA 局部剂量增加。这是由于碳 K 壳层相互作用和产生的电子短程增加所致。DNA 中的核心离子化,通过与局部相关的低能光和俄歇电子的核心空穴弛豫相结合,导致 DSB 的数量和复杂性增加。

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