Department of Nuclear Medicine and Radiobiology, Faculty of Medicine and Heath Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada J1H 5N4.
J Phys Chem B. 2013 Sep 5;117(35):10122-31. doi: 10.1021/jp405397m. Epub 2013 Aug 23.
The genotoxic effects of high-energy ionizing radiation have been largely attributed to the ionization of H2O leading to hydroxyl radicals and the ionization of DNA leading mostly to damage through base radical cations. However, the contribution of low-energy electrons (LEEs; ≤ 10 eV), which involves subionization events, has been considered to be less important than that of hydroxyl radicals and base radical cations. Here, we compare the ability of LEEs and high-energy X-ray photons to induce DNA damage using dried thin films of TpTpT trinucleotide as a simple and representative model for DNA damage. The main radiation-induced damage of TpTpT as measured by high-performance liquid chromatography (HPLC) with UV detection and HPLC coupled to tandem mass spectrometry analyses included thymine release (-Thy), strand breaks (pT, Tp, pTpT, TpTp, and TpT), and the formation of base modifications [5,6-dihydrothymine (5,6-dhT), 5-hydroxymethyluracil (5-hmU), and 5-formyluracil (5-fU)]. The global profile of products was very similar for both types of radiation indicating converging pathways of formation. The percent damage of thymine release, fragmentation, and base modification was 20, 19, and 61 for high-energy X-rays, respectively, compared to 35, 13, and 51 for LEEs (10 eV). Base release was significantly lower for X-rays. In both cases, phosphodiester bond cleavage gave mononucleotides (pT and Tp) and dinucleotides (pTpT and TpTp) containing a terminal phosphate as the major fragments. For base modifications, the ratio of reductive (5,6-dhT) to oxidative products (5-hmU plus 5-fU) was 0.9 for high-energy X-rays compared to 1.7 for LEEs. These results indicate that LEEs give a similar profile of products compared to ionizing radiation.
高能电离辐射的遗传毒性效应主要归因于 H2O 的电离导致羟基自由基的形成,以及 DNA 的电离主要导致碱基自由基阳离子的损伤。然而,低能电子(LEE;≤10 eV)的贡献被认为不如羟基自由基和碱基自由基阳离子重要,因为低能电子涉及亚电离事件。在这里,我们比较了 LEE 和高能 X 射线光子诱导 DNA 损伤的能力,使用 TpTpT 三核苷酸的干燥薄膜作为 DNA 损伤的简单和代表性模型。通过高效液相色谱(HPLC)与紫外检测和 HPLC 与串联质谱分析相结合,测量到 TpTpT 的主要辐射诱导损伤包括胸腺嘧啶释放(-Thy)、链断裂(pT、Tp、pTpT、TpTp 和 TpT)以及碱基修饰的形成[5,6-二氢胸腺嘧啶(5,6-dhT)、5-羟甲基尿嘧啶(5-hmU)和 5-甲酰基尿嘧啶(5-fU)]。两种类型的辐射产生的产物的整体谱非常相似,表明形成途径趋同。高能 X 射线诱导的胸腺嘧啶释放、片段化和碱基修饰的损伤百分比分别为 20%、19%和 61%,而 LEE(10 eV)分别为 35%、13%和 51%。X 射线诱导的碱基释放明显较低。在这两种情况下,磷酸二酯键的断裂产生了含有末端磷酸的单核核苷酸(pT 和 Tp)和二核苷酸(pTpT 和 TpTp)作为主要片段。对于碱基修饰,高能 X 射线产生的还原产物(5,6-dhT)与氧化产物(5-hmU 加 5-fU)的比值为 0.9,而 LEE 为 1.7。这些结果表明,LEE 与电离辐射产生相似的产物谱。