Altered growth and radiosensitivity in neural precursor cells subjected to oxidative stress
Altered growth and radiosensitivity in neural precursor cells subjected to oxidative stress
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DOI：
10.1080/09553000600887816
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发表时间：
2006-09-01
影响因子：
2.6
通讯作者：
Fike, John R.
中科院分区：
文献类型：
--
作者：
Limoli, Charles L.;Giedzinski, Erich;Fike, John R.
目的：为了确定氧化应激的变化是否可以增强神经前体细胞对电离辐射的敏感性，材料和方法：使用两种策略，即通过操纵细胞培养密度内源性地调节氧化应激，或通过直接加入过氧化氢外源性地调节氧化应激。通过低密度生长增加内源性氧化应激的细胞通常在照射后表现出生长抑制。然而，长期外源性氧化处理的细胞表现出增加的敏感性质子和g-照射相比，未经处理的控制。使用酶活力测定证实了经受氧化条件的辐照培养物的存活率降低，并且在一定剂量范围（1-5戈伊）和辐照后再接种密度下观察到（20-200 K/板）。总的来说，我们的结果进一步支持了氧化还原状态在神经前体细胞功能调节中的重要性，并提示氧化应激可通过不同的机制抑制细胞的增殖潜能。这可能会危及生存，并且在过量的外源性氧化剂可能占主导地位的条件下，对辐射的敏感性可能会增强。
Purpose: To determine whether changes in oxidative stress could enhance the sensitivity of neural precursor cells to ionizing radiation.Materials and methods: Two strategies were used whereby oxidative stress was modulated endogenously, through manipulation cell culture density, or exogenously, through direct addition of hydrogen peroxide.Results: Cells subjected to increased endogenous oxidative stress through low-density growth routinely exhibited an inhibition of growth following irradiation. However, cells subjected to chronic exogenous oxidative treatments showed increased sensitivity to proton and g-irradiation compared to untreated controls. Reduced survival of irradiated cultures subjected to oxidizing conditions was corroborated using enzymatic viability assays, and was observed over a range of doses (1-5 Gy) and post-irradiation re-seeding densities (20-200 K/plate).Conclusions: Collectively our results provide further support for the importance of redox state in the regulation of neural precursor cell function, and suggest that oxidative stress can inhibit the proliferative potential of cells through different mechanisms. This is likely to compromise survival and under conditions where excess exogenous oxidants might predominate, sensitivity to irradiation may be enhanced.