Reactive oxygen species (ROS) are a group of short-lived, highly reactive, oxygen-containing molecules that can induce DNA damage and affect the DNA damage response (DDR). There is unequivocal pre-clinical and clinical evidence that ROS influence the genotoxic stress caused by chemotherapeutics agents and ionizing radiation. Recent studies have provided mechanistic insight into how ROS can also influence the cellular response to DNA damage caused by genotoxic therapy, especially in the context of Double Strand Breaks (DSBs). This has led to the clinical evaluation of agents modulating ROS in combination with genotoxic therapy for cancer, with mixed success so far. These studies point to context dependent outcomes with ROS modulator combinations with Chemotherapy and radiotherapy, indicating a need for additional pre-clinical research in the field. In this review, we discuss the current knowledge on the effect of ROS in the DNA damage response, and its clinical relevance.

活性氧 (ROS) 是一组短寿命、高活性的含氧分子，可诱导 DNA 损伤并影响 DNA 损伤反应 (DDR)。有明确的临床前和临床证据表明，ROS 影响化疗药物和电离辐射引起的基因毒性应激。最近的研究提供了关于 ROS 如何影响细胞对基因毒性治疗引起的 DNA 损伤的反应的机制见解，特别是在双链断裂 (DSB) 的背景下。这导致了对 ROS 调节剂与癌症基因毒性疗法相结合的临床评估，迄今为止取得了不同程度的成功。这些研究指出 ROS 调节剂与化疗和放疗组合的结果依赖于环境，表明需要在该领域进行额外的临床前研究。在这篇综述中，我们讨论了目前关于 ROS 在 DNA 损伤反应中的影响及其临床相关性的知识。