放射性药物治疗（RPT）正在发展成为一种有前景的癌症治疗策略。随着人们对俄歇电子等短程粒子的兴趣不断增长，了解脱氧核糖核酸 (DNA) 水平的剂量响应关系变得至关重要。在本研究中，我们使用 Geant4-DNA 工具包来评估俄歇电子发射同位素 I-125 造成的 DNA 损伤。我们将短 B 型 DNA (B-DNA) 几何结构中每个碱基对位置的能量沉积和单链断裂 (SSB) 产量与现有模拟和实验数据进行了比较，同时考虑了物理直接命中和化学间接命中。此外，我们还评估了我们的高分辨率 B-DNA 靶标与之前发布的简单 B-DNA 几何结构之间的剂量差异。总体而言，我们对 I-125 衰变的 SSB 产量的基准测试结果与模拟和实验数据表现出良好的一致性。然后，我们利用该模拟评估了治疗诊断 Br-77 标记的聚 ADP 核糖聚合酶 (PARP) 抑制剂放射性药物引起的 SSB 和双链断裂 (DSB) 产量。结果表明，在产生 SSB 和 DSB 方面，化学间接撞击比物理直接撞击占主导地位。这项研究为未来研究 RPT 的纳米剂量特性奠定了基础。

Radiopharmaceutical therapy (RPT) is evolving as a promising strategy for treating cancer. As interest grows in short-range particles, like Auger electrons, understanding the dose-response relationship at the deoxyribonucleic acid (DNA) level has become essential. In this study, we used the Geant4-DNA toolkit to evaluate DNA damage caused by the Auger-electron-emitting isotope I-125. We compared the energy deposition and single strand break (SSB) yield at each base pair location in a short B-form DNA (B-DNA) geometry with existing simulation and experimental data, considering both physical direct and chemical indirect hits. Additionally, we evaluated dosimetric differences between our high-resolution B-DNA target and a previously published simple B-DNA geometry. Overall, our benchmarking results for SSB yield from I-125 decay exhibited good agreement with both simulation and experimental data. Using this simulation, we then evaluated the SSB and double strand break (DSB) yields caused by a theranostic Br-77-labeled poly ADP ribose polymerase (PARP) inhibitor radiopharmaceutical. The results indicated a predominant contribution of chemical indirect hits over physical direct hits in generating SSB and DSB. This study lays the foundation for future investigations into the nano-dosimetric properties of RPT.