Ionizing radiation has been shown to cause induced genomic instability (IGI), which is defined as a persistently increased rate of genomic damage in the progeny of the exposed cells. In this study, IGI was investigated by exposing human SH-SY5Y neuroblastoma cells to hydroxyurea and zeocin, two chemicals mimicking different DNA-damaging effects of ionizing radiation. The aim was to explore whether IGI was associated with persistent mitochondrial dysfunction. Changes to mitochondrial function were assessed by analyzing mitochondrial superoxide production, mitochondrial membrane potential, and mitochondrial activity. The formation of micronuclei was used to determine immediate genetic damage and IGI. Measurements were performed either immediately, 8 days, or 15 days following exposure. Both hydroxyurea and zeocin increased mitochondrial superoxide production and affected mitochondrial activity immediately after exposure, and mitochondrial membrane potential was affected by zeocin, but no persistent changes in mitochondrial function were observed. IGI became manifested 15 days after exposure in hydroxyurea-exposed cells. In conclusion, immediate responses in mitochondrial function did not cause persistent dysfunction of mitochondria, and this dysfunction was not required for IGI in human neuroblastoma cells.

电离辐射已被证明会导致诱导基因组不稳定性 (IGI)，其定义为暴露细胞后代中基因组损伤率持续增加。在这项研究中，通过将人类 SH-SY5Y 神经母细胞瘤细胞暴露于羟基脲和 zeocin 来研究 IGI，这两种化学物质模拟了电离辐射对 DNA 的不同破坏作用。目的是探索 IGI 是否与持续性线粒体功能障碍有关。通过分析线粒体超氧化物的产生、线粒体膜电位和线粒体活性来评估线粒体功能的变化。微核的形成用于确定直接的遗传损伤和 IGI。在暴露后立即、8 天或 15 天进行测量。羟基脲和zeocin在暴露后立即增加线粒体超氧化物的产生并影响线粒体活性，并且线粒体膜电位受到zeocin的影响，但未观察到线粒体功能的持续变化。IGI 在暴露于羟基脲的细胞中 15 天后出现。总之，线粒体功能的即时反应不会导致线粒体的持续功能障碍，并且这种功能障碍对于人神经母细胞瘤细胞中的 IGI 不是必需的。