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首页> 美国卫生研究院文献>Redox Biology >Characterizing low dose and dose rate effects in rodent and human neural stem cells exposed to proton and gamma irradiation
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Characterizing low dose and dose rate effects in rodent and human neural stem cells exposed to proton and gamma irradiation

机译：表征质子和伽马射线辐照的啮齿动物和人类神经干细胞的低剂量和剂量率效应

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Past work has shown that exposure to gamma rays and protons elicit a persistent oxidative stress in rodent and human neural stem cells (hNSCs). We have now adapted these studies to more realistic exposure scenarios in space, using lower doses and dose rates of these radiation modalities, to further elucidate the role of radiation-induced oxidative stress in these cells. Rodent neural stem and precursor cells grown as neurospheres and human neural stem cells grown as monolayers were subjected to acute and multi-dosing paradigms at differing dose rates and analyzed for changes in reactive oxygen species (ROS), reactive nitrogen species (RNS), nitric oxide and superoxide for 2 days after irradiation. While acute exposures led to significant changes in both cell types, hNSCs in particular, exhibited marked and significant elevations in radiation-induced oxidative stress. Elevated oxidative stress was more significant in hNSCs as opposed to their rodent counterparts, and hNSCs were significantly more sensitive to low dose exposures in terms of survival. Combinations of protons and γ-rays delivered as lower priming or higher challenge doses elicited radioadaptive changes that were associated with improved survival, but in general, only under conditions where the levels of reactive species were suppressed compared to cells irradiated acutely. Protective radioadaptive effects on survival were eliminated in the presence of the antioxidant N-acetylcysteine, suggesting further that radiation-induced oxidative stress could activate pro-survival signaling pathways that were sensitive to redox state. Data corroborates much of our past work and shows that low dose and dose rate exposures elicit significant changes in oxidative stress that have functional consequences on survival.
机译：过去的工作表明，接触γ射线和质子会在啮齿动物和人类神经干细胞（hNSC）中引起持续的氧化应激。现在，我们已使用较低剂量和这些辐射方式的剂量率使这些研究适应更现实的太空暴露场景，以进一步阐明辐射诱导的氧化应激在这些细胞中的作用。以不同的剂量率对作为神经球体生长的啮齿动物神经干细胞和前体细胞以及作为单层生长的人类神经干细胞进行不同剂量的急性和多剂量模式研究，并分析活性氧（ROS），活性氮（RNS），硝酸的变化辐照后2天内氧化氮和超氧化物。急性暴露导致两种细胞类型发生显着变化，特别是hNSCs在辐射诱导的氧化应激中表现出明显的显着升高。与啮齿类动物相比，hNSCs中较高的氧化应激更为显着，就生存而言，hNSCs对低剂量暴露更为敏感。较低的启动剂量或较高的激发剂量所传递的质子和γ射线组合会引起放射适应性变化，与存活率提高相关，但通常，仅在反应性物种水平与急性照射的细胞相比受到抑制的条件下。在抗氧化剂N-乙酰半胱氨酸的存在下消除了对生存的保护性放射适应作用，这进一步表明辐射诱导的氧化应激可以激活对氧化还原状态敏感的促存活信号通路。数据证实了我们过去的许多工作，并表明低剂量和高剂量率暴露会引起氧化应激的显着变化，从而对生存产生功能性影响。

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