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电离辐射诱导和修复DNA双链断裂的机制:一些矛盾之处。

Mechanisms of induction and repair of DNA double-strand breaks by ionizing radiation: some contradictions.

作者信息

Hagen U

机构信息

GSF-Institut für Strahlenbiologie, Neuherberg, Oberschleissheim, Germany.

出版信息

Radiat Environ Biophys. 1994;33(1):45-61. doi: 10.1007/BF01255273.

Abstract

The various aspects of formation and repair of radiation-induced double-strand breaks (DSB) are summarized. Concerning the structure of DSB found in irradiated cells, enzymatic and microdosimetric analysis hints at complex damage of the DNA structure at the position of a DSB. With increasing LET, the DSB damage may be more complex than that induced by low-LET irradiation. Most of the DSB are repaired in the irradiated cell; apparently the kinetics of DSB repair and the fraction of unrejoined DSB determine cell survival or cell death. We do not know the details of the complex machinery of DSB repair; certainly recombination processes are involved, but there are still contradictions between our current knowledge about the mechanisms of recombinational DSB repair and the observed kinetics.

摘要

本文总结了辐射诱导双链断裂(DSB)的形成和修复的各个方面。关于在受辐照细胞中发现的DSB结构,酶学和微剂量分析表明DSB位置的DNA结构存在复杂损伤。随着传能线密度(LET)的增加,DSB损伤可能比低LET辐射诱导的损伤更复杂。大多数DSB在受辐照细胞中得到修复;显然,DSB修复的动力学和未连接的DSB比例决定了细胞存活或死亡。我们尚不清楚DSB修复复杂机制的细节;重组过程肯定参与其中,但我们目前对重组DSB修复机制的了解与观察到的动力学之间仍存在矛盾。

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