Relief of delayed oxidative stress by ascorbic acid can suppress radiation-induced cellular senescence in mammalian fibroblast cells
Relief of delayed oxidative stress by ascorbic acid can suppress radiation-induced cellular senescence in mammalian fibroblast cells
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DOI：
10.1016/j.mad.2015.05.002
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发表时间：
2015-03-01
影响因子：
5.3
通讯作者：
Watanabe, Masami
中科院分区：
文献类型：
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作者：
Kobashigawa, Shinko;Kashino, Genro;Watanabe, Masami
电离辐射诱导的细胞衰老被认为是由无法修复的核DNA损伤引起的。然而，在这里，我们发现，辐射诱导延迟增加细胞内的氧化应激辐射后。我们调查是否延迟氧化应激的救济抗坏血酸将抑制辐射诱导的细胞衰老在叙利亚金黄地鼠胚胎（SHE）细胞。我们观察到，氧化应激水平在照射后不久急剧增加，然后下降到非照射细胞的水平，并再次增加，在照射后第3天达到峰值。我们发现，X射线照射后细胞衰老的诱导减少沿着抑制延迟诱导的氧化应激与抗坏血酸治疗，但不是当氧化应激发生后立即照射。此外，抗坏血酸处理抑制p53积累在照射后3天。我们的数据表明，细胞内氧化应激水平的延迟增加在辐射诱导的细胞衰老的过程中起着重要的作用，通过p53积累。(C)2015爱思唯尔爱尔兰有限公司版权所有。
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.