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- W2034771304 abstract "Reactive oxygen species (ROS) is thought to play an important role in cell signaling of apoptosis, necrosis, and proliferation. Light irradiation increases mitochondrial reactive oxygen species (ROS) production and mediates its intracellular signaling by adjusting the redox potential in tumor cells. Mitochondria are the main source of ROS in the living cell. Superoxide anions (0<sub>2</sub><sup>-</sup> are likely the first ROS generated in the mitochondria following radiation damage, and then convert to hydrogen peroxide (H<sub>2</sub>0<sub>2</sub>), hydroxyl radical (•OH), and singlet oxygen (<sup>1</sup>0<sub>2</sub>), etc. Conventional methods for research ROS production in mitochondria mostly use isolated mitochondria rather than mitochondria in living cells. In this study, a highly selective probe to detect mitochondrial 0<sub>2</sub><sup>-</sup> in live cells, MitoSOX<sup>TM </sup> Red, was applied to quantify the mitochondrial ROS production in human lung adenocarcinoma cells (ASTC-a-1) with laser scanning microscope (LSM) after ultraviolet C (UVC) and He-Ne laser irradiation. Dichiorodihydrofluoresein diacetate (DCFHDA), a common used fluorescent probe for ROS detection without specificity, were used as a comparison to image the ROS production. The fluorescent image of MItoSOX<sup>TM</sup> Red counterstained with MitoTracker Deep Red 633, a mitochondria selective probe, shows that the mitochondrial ROS production increases distinctly after UVC and He-Ne laser irradiation. DCFH-DA diffuses labeling throughout the cell though its fluorescence increases markedly too. In conclusion, the fluorescent method with MitoSOX<sup>TM</sup> Red reagent is proved to be a promising technique to research the role of ROS in radiation induced apoptosis." @default.
- W2034771304 created "2016-06-24" @default.
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- W2034771304 date "2006-09-01" @default.
- W2034771304 modified "2023-09-25" @default.
- W2034771304 title "Detection of irradiation induced reactive oxygen species production in live cells" @default.
- W2034771304 doi "https://doi.org/10.1117/12.710703" @default.
- W2034771304 hasPublicationYear "2006" @default.
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