Fractionated exposure to low doses of ionizing radiation results in accumulation of DNA damage in mouse spleen tissue and activation of apoptosis in a p53/Atm-independent manner.
Fractionated exposure to low doses of ionizing radiation results in accumulation of DNA damage in mouse spleen tissue and activation of apoptosis in a p53/Atm-independent manner.
复制标题
DOI：
10.1080/09553002.2017.1231943
复制
发表时间：
2017-03
影响因子：
2.6
通讯作者：
Kovalchuk O
中科院分区：
文献类型：
--
作者：
Koturbash I;Merrifield M;Kovalchuk O
虽然高剂量电离辐射（IR）的影响已经得到了较好的表征，但对长时间暴露于低剂量辐射的细胞反应的分子机制仍未得到充分研究。本文研究了0.1-0.5Gy剂量范围内x射线对C57BL/6雄性小鼠脾脏组织DNA损伤和凋亡反应的影响。对初始暴露于0.1 Gy IR的反应的特征是DNA损伤增加和细胞凋亡水平升高。随后的暴露（累积剂量为0.2和0.3 Gy）导致适应性反应样变化，表现为增殖和凋亡反应增加。在0.4和0.5 Gy的累积剂量下，DNA损伤累积，细胞凋亡和细胞凋亡相关蛋白重新激活。此外，辐射引起的不可逆损伤的脾细胞可以通过p38的激活而发生凋亡，而p38的激活并不一定涉及Atm/p53通路。分次暴露于低剂量x射线导致小鼠脾脏DNA损伤积累，并以p53/ atm不依赖的方式诱导凋亡反应。需要进一步的研究来了解长时间暴露于IR下的细胞反应和p38早期诱导的结果和分子机制。
While the effects of high doses of ionizing radiation (IR) are relatively well characterized, the molecular mechanisms underlying cellular responses to prolonged exposure to low doses of radiation remain largely under-investigated. Here, we addressed the DNA damage and apoptotic response in the spleen tissue of C57BL/6 male mice after fractionated exposure to X-rays within the 0.1–0.5Gy dose range. The response to initial exposure to 0.1 Gy of IR was characterized by increased DNA damage and elevated levels of apoptosis. Subsequent exposures (cumulative doses of 0.2 and 0.3 Gy) resulted in adaptive response-like changes, represented as increased proliferation and apoptotic response. Cumulative doses of 0.4 and 0.5 Gy were characterized by accumulation of DNA damage and reactivation of apoptosis and apoptosis-related proteins. Additionally, spleen cells with irreversible damage caused by radiation can undergo apoptosis via activation of p38, which does not necessarily involve the Atm/p53 pathway. Fractionated exposure to low doses of X-rays resulted in accumulation of DNA damage in the murine spleen and induction of apoptotic response in p53/Atm-independent manner. Further studies are needed to understand the outcomes and molecular mechanisms underlying cellular responses and early induction of p38 in response to prolonged exposure to IR.
登录
查看更多内容
影响因子：
2.6
作者：
Li, W;Wang, GJ;Cai, L
通讯作者：
Cai, L
影响因子：
8
作者：
Morgan, WF
通讯作者：
Morgan, WF
影响因子：
5.7
作者：
Klokov, Dmitry;MacPhail, Susan M.;Olive, Peggy L.
通讯作者：
Olive, Peggy L.
影响因子：
4.3
作者：
Koturbash, Igor;Zemp, Franz J.;Kovalchuk, Olga
通讯作者：
Kovalchuk, Olga
影响因子：
168.9
作者：
Kamiya, Kenji;Ozasa, Kotaro;Wakeford, Richard
通讯作者：
Wakeford, Richard