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  • 标题:Potential relationship between the biological effects of low-dose irradiation and mitochondrial ROS production
  • 本地全文:下载
  • 作者:Kasumi Kawamura ; Fei Qi ; Junya Kobayashi
  • 期刊名称:Journal of Radiation Research
  • 印刷版ISSN:0449-3060
  • 电子版ISSN:1349-9157
  • 出版年度:2018
  • 卷号:59
  • 期号:suppl_2
  • 页码:91-97
  • DOI:10.1093/jrr/rrx091
  • 摘要:Exposure to ionizing radiation (IR) induces various types of DNA damage, of which DNA double-strand breaks are the most severe, leading to genomic instability, tumorigenesis, and cell death. Hence, cells have developed DNA damage responses and repair mechanisms. IR also causes the accumulation of endogenous reactive oxidative species (ROS) in the irradiated cells. Upon exposure to low-dose irradiation, the IR-induced biological effects mediated by ROS were relatively more significant than those mediated by DNA damage. Accumulating evidence suggests that such increase in endogenous ROS is related with mitochondria change in irradiated cells. Thus, in this review we focused on the mechanism of mitochondrial ROS production and its relationship to the biological effects of IR. Exposure of mammalian cells to IR stimulates an increase in the production of endogenous ROS by mitochondria, which potentially leads to mitochondrial dysfunction. Since the remains of damaged mitochondria could generate or leak more ROS inside the cell, the damaged mitochondria are removed by mitophagy. The disruption of this pathway, involved in maintaining mitochondrial integrity, could lead to several disorders (such as neurodegeneration) and aging. Thus, further investigation needs to be performed in order to understand the relationship between the biological effects of low-dose IR and mitochondrial integrity. © The Author(s) 2018. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology.
  • 关键词:ROS;low-dose irradiation;mitochondria;mitophagy;oxidative damage
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