Relief of delayed oxidative stress by ascorbic acid can suppress radiation-induced cellular senescence in mammalian fibroblast cells

被引:13
|
作者
Kobashigawa, Shinko [1 ]
Kashino, Genro [2 ]
Mori, Hiromu [1 ]
Watanabe, Masami [3 ]
机构
[1] Oita Univ, Sch Med, Dept Radiol, Yufu City, Oita 8795593, Japan
[2] Oita Univ, Sch Med, Adv Mol Imaging Ctr, Yufu City, Oita 8795593, Japan
[3] Kyoto Univ, Ctr Radiat Biol, Kyoto 606, Japan
基金
日本学术振兴会;
关键词
Ionizing radiation; Oxidative stress; Radiation-induced cellular senescence; Ascorbic acid; OXYGEN SPECIES PRODUCTION; LIFE-SPAN; GROWTH ARREST; SUPEROXIDE-DISMUTASE; P53; EXTENSION; OVEREXPRESSION; MITOCHONDRIA; INSTABILITY; ACTIVATION;
D O I
10.1016/j.mad.2015.05.002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ionizing radiation-induced cellular senescence is thought to be caused by nuclear DNA damage that cannot be repaired. However, here we found that radiation induces delayed increase of intracellular oxidative stress after irradiation. We investigated whether the relief of delayed oxidative stress by ascorbic acid would suppress the radiation-induced cellular senescence in Syrian golden hamster embryo (SHE) cells. We observed that the level of oxidative stress was drastically increased soon after irradiation, then declined to the level in non-irradiated cells, and increased again with a peak on day 3 after irradiation. We found that the inductions of cellular senescence after X-irradiation were reduced along with suppression of the delayed induction of oxidative stress by treatment with ascorbic acid, but not when oxidative stress occurred immediately after irradiation. Moreover, treatment of ascorbic acid inhibited p53 accumulation at 3 days after irradiation. Our data suggested a delayed increase of intracellular oxidative stress levels plays an important role in the process of radiation-induced cellular senescence by p53 accumulation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:65 / 71
页数:7
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