Redox changes induced in hippocampal precursor cells by heavy ion irradiation
Redox changes induced in hippocampal precursor cells by heavy ion irradiation
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DOI：
10.1007/s00411-006-0077-9
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发表时间：
2007-06-01
影响因子：
1.7
通讯作者：
Fike, J. R.
中科院分区：
文献类型：
--
作者：
Limoli, C. L.;Giedzinski, E.;Fike, J. R.
海马体前体在整个生命过程中保持增殖和分化的能力，它们的后代，未成熟的神经元，可以经历神经发生，这一过程被认为对维持生物体的认知健康很重要。包括辐照在内的各种压力已被证明会耗尽神经前体细胞，这种影响会抑制神经发生，并与认知障碍的发作有关。我们过去的工作表明，暴露于x射线或质子的神经前体细胞表现出长时间的氧化应激增加，我们假设这是在辐照和其他应激后调节这些细胞功能的关键因素。在这里，我们报告了与低LET辐射（x射线，质子）相比，用高线性能量转移（LET） 1 GeV/核子Fe-56离子照射海马前体细胞会导致明显更高水平的氧化应激。以1戈瑞的铁-56离子照射可引起的活性氧水平较未照射的对照组高出两至五倍，而在较低剂量下(
Hippocampal precursors retain the capacity to proliferate and differentiate throughout life, and their progeny, immature neurons, can undergo neurogenesis, a process believed to be important in maintaining the cognitive health of an organism. A variety of stresses including irradiation have been shown to deplete neural precursor cells, an effect that inhibits neurogenesis and is associated with the onset of cognitive impairments. Our past work has shown that neural precursor cells exposed to X-rays or protons exhibit a prolonged increase in oxidative stress, a factor we hypothesize to be critical in regulating the function of these cells after irradiation and other stresses. Here we report that irradiation of hippocampal precursor cells with high-linear energy transfer (LET) 1 GeV/nucleon Fe-56 ions leads to significantly higher levels of oxidative stress when compared to lower LET radiations (Xrays, protons). Irradiation with 1 Gy of Fe-56 ions elicits twofold to fivefold higher levels of reactive oxygen species (ROS) compared to unirradiated controls, and at lower doses (