Abstract：
5-Fluorouracil is now routinely used in chemo- and radiotherapy. Incorporated within DNA, the molecule is bound to the sugar backbone, forming the 5-fluorouridine sub-unit investigated in the present work. For the clinical usage of the latter, no information exists on the mechanisms that control the radiosensitizing effect at the molecular level. As low energy (< 12 eV) electrons are abundantly produced along the radiation tracks during cancer treatment using beams of high energy particles, we study how these ballistic secondary electrons damage the sensitizing molecule. The salient result from our study shows that the N-glycosidic bonds are principally affected with a cross-section of approximately two orders of magnitude higher than the canonical thymidine, reflecting to some degree the surviving factor of radiation-treated carcinoma cells with and without 5-fluorouracil incorporation. This result may help in the comprehension of the radiosensitizing effect of the fluoro-substituted thymidine in DNA.
摘要：
5-氟尿嘧啶现在常规用于化学疗法和放射疗法。结合在DNA中，分子与糖骨架结合，形成本工作中研究的5-氟尿嘧啶亚基。对于后者的临床使用，没有关于在分子水平上控制放射增敏作用的机制的信息。由于在癌症治疗期间使用高能粒子束沿着辐射轨道大量产生低能量(<12eV)电子,我们研究这些弹道二次电子是如何破坏敏化分子的。我们研究的显着结果表明，N-糖苷键主要受到比经典胸苷高大约两个数量级的横截面的影响。在一定程度上反映了有或没有5-氟尿嘧啶掺入的放射治疗癌细胞的存活因子。此结果可能有助于理解DNA中氟取代的胸苷的放射增敏作用。
