Mitochondria-Targeted Superoxide Dismutase (SOD2) Regulates Radiation Resistance and Radiation Stress Response in HeLa Cells

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  • HOSOKI Ayaka
    Department of Biological Sciences, Graduate School of Science, Kyoto University
  • YONEKURA Shin-Ichiro
    Department of Biological Sciences, Graduate School of Science, Kyoto University
  • ZHAO Qing-Li
    Department of Radiological Sciences, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
  • WEI Zheng-Li
    Department of Radiological Sciences, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
  • TAKASAKI Ichiro
    Division of Molecular Genetics Research, Life Science Research Center, University of Toyama
  • TABUCHI Yoshiaki
    Division of Molecular Genetics Research, Life Science Research Center, University of Toyama
  • WANG Li-Li
    Department of Biological Sciences, Graduate School of Science, Kyoto University
  • HASUIKE Shiga
    Department of Radiation Oncology and Image-applied Therapy, Graduate School of Medicine, Kyoto University
  • NOMURA Takaharu
    Low Dose Radiation Research Center, Central Research Institute of Electric Power Industry
  • TACHIBANA Akira
    Department of Biology, Faculty of Science, Ibaraki University
  • HASHIGUCHI Kazunari
    Department of Biological Sciences, Graduate School of Science, Kyoto University
  • YONEI Shuji
    Department of Biological Sciences, Graduate School of Science, Kyoto University
  • KONDO Takashi
    Department of Radiological Sciences, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
  • ZHANG-AKIYAMA Qiu-Mei
    Department of Biological Sciences, Graduate School of Science, Kyoto University

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Reactive oxygen species (ROS) act as a mediator of ionizing radiation-induced cellular damage. Previous studies have indicated that MnSOD (SOD2) plays a critical role in protection against ionizing radiation in mammalian cells. In this study, we constructed two types of stable HeLa cell lines overexpressing SOD2, HeLa S3/SOD2 and T-REx HeLa/SOD2, to elucidate the mechanisms underlying the protection against radiation by SOD2. SOD2 overexpression in mitochondria enhanced the survival of HeLa S3 and T-REx HeLa cells following γ-irradiation. The levels of γH2AX significantly decreased in HeLa S3/SOD2 and T-REx HeLa/SOD2 cells compared with those in the control cells. MitoSoxTM Red assays showed that both lines of SOD2-expressing cells showed suppression of the superoxide generation in mitochondria. Furthermore, flow cytometry with a fluorescent probe (2',7'-dichlorofluorescein) revealed that the cellular levels of ROS increased in HeLa S3 cells during post-irradiation incubation, but the increase was markedly attenuated in HeLa S3/SOD2 cells. DNA microarray analysis revealed that, of 47,000 probe sets analyzed, 117 and 166 probes showed more than 2-fold changes after 5.5 Gy of γ-irradiation in control and HeLa S3/SOD2 cells, respectively. Pathway analysis revealed different expression profiles in irradiated control cells and irradiated SOD2-overexpressing cells. These results indicate that SOD2 protects HeLa cells against cellular effects of γ-rays through suppressing oxidative stress in irradiated cells caused by ROS generated in the mitochondria and through regulating the expression of genes which play a critical role in protection against ionizing radiation.

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