Hofer K G
Institute of Molecular Biophysics, Florida State University, Tallahassee 32306, USA.
Acta Oncol. 1996;35(7):789-96. doi: 10.3109/02841869609104028.
Radionuclide decay by electron capture and/or internal conversion is accompanied by complex atomic vacancy cascades and emission of low-energy electrons, resulting in a highly charged daughter atom and a high density of electron irradiation in the immediate vicinity of the decay site. The molecular and cellular consequences of such decay events include DNA strand breaks, mutations, chromosome aberrations, malignant transformation, division delay, and cell death. Damage to cells depends largely on the intracellular location of the radionuclide. Decays outside the cell nucleus produce low-LET-type radiation effects (RBE approximately 1). In contrast, decays in DNA cause pronounced high-LET-type effects (RBE approximately 7-9). However, recent studies suggest that even for DNA-associated Auger emitters cell damage can be modified to resemble the pattern observed with low-LET radiations. These findings indicate that the molecular and cellular mechanism(s) responsible for the cytotoxic effects of Auger emitters remain obscure.
通过电子俘获和/或内转换进行的放射性核素衰变伴随着复杂的原子空位级联和低能电子的发射，导致产生一个高电荷的子原子，并在衰变位点附近形成高密度的电子辐射。此类衰变事件对分子和细胞的影响包括DNA链断裂、突变、染色体畸变、恶性转化、分裂延迟和细胞死亡。对细胞的损伤在很大程度上取决于放射性核素在细胞内的位置。在细胞核外发生的衰变产生低传能线密度（LET）类型的辐射效应（相对生物效应约为1）。相比之下，在DNA中发生的衰变会导致明显的高LET类型效应（相对生物效应约为7 - 9）。然而，最近的研究表明，即使对于与DNA相关的俄歇电子发射体，细胞损伤也可以被改变，使其类似于低LET辐射所观察到的模式。这些发现表明，负责俄歇电子发射体细胞毒性作用的分子和细胞机制仍不清楚。
