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• W2059090712 startingPage "455" @default.
• W2059090712 abstract "Radiation-induced cell death is thought to be caused by nuclear DNA damage that cannot be repaired. However, in this study we found that a delayed increase of mitochondrial reactive oxygen species (ROS) is responsible for some of the radiation-induced cell death in normal human fibroblast cells. We have previously reported that there is a delayed increase of mitochondrial (·)O2(-), measured using MitoSOX™ Red reagent, due to gamma irradiation. This is dependent on Drp1 localization to mitochondria. Here, we show that knockdown of Drp1 expression reduces the level of DNA double-strand breaks (DSBs) remaining 3 days after 6 Gy irradiation. Furthermore, cells with knockdown of Drp1 expression are more resistant to gamma radiation. We then tested whether the delayed increase of ROS causes DNA damage. The antioxidant, 2-glucopyranoside ascorbic acid (AA-2G), was applied before or after irradiation to inhibit ROS production during irradiation or to inhibit delayed ROS production from mitochondria. Interestingly, 1 h after exposure, the AA-2G treatment reduced the level of DSBs remaining 3 days after 6 Gy irradiation. In addition, irradiated AA-2G-treated cells were more resistant to radiation than the untreated cells. These results indicate that delayed mitochondrial ROS production may cause some of the cell death after irradiation." @default.
• W2059090712 created "2016-06-24" @default.
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• W2059090712 date "2015-03-25" @default.
• W2059090712 modified "2023-09-27" @default.
• W2059090712 title "Ionizing Radiation-Induced Cell Death Is Partly Caused by Increase of Mitochondrial Reactive Oxygen Species in Normal Human Fibroblast Cells" @default.
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• W2059090712 doi "https://doi.org/10.1667/rr13772.1" @default.
• W2059090712 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25807320" @default.
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