Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury.
Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury.
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DOI：
10.1016/j.canlet.2011.12.012
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发表时间：
2012-12-31
期刊：
影响因子：
9.7
通讯作者：
Pain D
中科院分区：
文献类型：
--
作者：
Azzam EI;Jay-Gerin JP;Pain D
细胞暴露于电离辐射导致氧化事件，通过辐射与目标大分子的直接相互作用或通过水辐解产物改变原子结构。此外，氧化损伤可以通过氧化还原调节的细胞间通讯机制从靶向细胞扩散到邻近的非靶向旁观者细胞。为了科普诱发的压力和氧化还原环境的变化，生物体在分子、细胞和组织水平上引起短暂的反应，以抵消辐射的毒性效应。在暴露期间和暴露后不久，代谢途径被诱导。根据辐射剂量、剂量率和质量，这些保护机制可能足以或可能不足以科普压力。当有害影响超过稳态生化过程时，诱导的生物学变化持续存在，并可能传播到后代细胞。活性氧和氮的生理水平在许多细胞功能中起着关键作用。在辐照细胞中，由于氧化代谢和慢性炎症反应的扰动，这些活性物质的水平可能会增加，从而导致电离辐射暴露对基因组稳定性的长期影响。在这里，除了水辐解对DNA损伤的直接生物学效应外，我们还讨论了线粒体在电离辐射延迟结果中的作用。线粒体功能的缺陷导致加速老化和许多病理条件。不同类型的辐射在其线性能量传递（LET）的属性不同，我们讨论了它们对线粒体生理学的各个方面的影响。这些包括对线粒体DNA、线粒体蛋白输入以及代谢和抗氧化酶的短期和长期体外和体内影响。
Cellular exposure to ionizing radiation leads to oxidizing events that alter atomic structure through direct interactions of radiation with target macromolecules or via products of water radiolysis. Further, the oxidative damage may spread from the targeted to neighboring, non-targeted bystander cells through redox-modulated intercellular communication mechanisms. To cope with the induced stress and the changes in the redox environment, organisms elicit transient responses at the molecular, cellular and tissue levels to counteract toxic effects of radiation. Metabolic pathways are induced during and shortly after the exposure. Depending on radiation dose, dose-rate and quality, these protective mechanisms may or may not be sufficient to cope with the stress. When the harmful effects exceed those of homeostatic biochemical processes, induced biological changes persist and may be propagated to progeny cells. Physiological levels of reactive oxygen and nitrogen species play critical roles in many cellular functions. In irradiated cells, levels of these reactive species may be increased due to perturbations in oxidative metabolism and chronic inflammatory responses, thereby contributing to the long-term effects of exposure to ionizing radiation on genomic stability. Here, in addition to immediate biological effects of water radiolysis on DNA damage, we also discuss the role of mitochondria in the delayed outcomes of ionization radiation. Defects in mitochondrial functions lead to accelerated aging and numerous pathological conditions. Different types of radiation vary in their linear energy transfer (LET) properties, and we discuss their effects on various aspects of mitochondrial physiology. These include short and long-term in vitro and in vivo effects on mitochondrial DNA, mitochondrial protein import and metabolic and antioxidant enzymes.
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影响因子：
2
作者：
Autsavapromporn N;De Toledo SM;Buonanno M;Jay-Gerin JP;Harris AL;Azzam EI
通讯作者：
Azzam EI
影响因子：
1.7
作者：
Boucher, Didier;Testard, Isabelle;Averbeck, Dietrich
通讯作者：
Averbeck, Dietrich
影响因子：
3.4
作者：
Azzam, EI;deToledo, SM;Mitchel, REJ
通讯作者：
Mitchel, REJ
影响因子：
3.9
作者：
Ammendola, R;Ruocchio, MR;Cimino, F
通讯作者：
Cimino, F
影响因子：
2.6
作者：
Aypar, Umut;Morgan, William F.;Baulch, Janet E.
通讯作者：
Baulch, Janet E.