Accidental exposure to ionizing radiation is a serious concern to human life. Studies on the mitigation of side effects following exposure to accidental radiation events are ongoing. Recent studies have shown that radiation can activate several signaling pathways, leading to changes in the metabolism of free radicals including reactive oxygen species (ROS) and nitric oxide (NO). Cellular and molecular mechanisms show that radiation can cause disruption of normal reduction/oxidation (redox) system. Mitochondria malfunction following exposure to radiation and mutations in mitochondria DNA (mtDNA) have a key role in chronic oxidative stress. Furthermore, exposure to radiation leads to infiltration of inflammatory cells such as macrophages, lymphocytes and mast cells, which are important sources of ROS and NO. These cells generate free radicals via upregulation of some pro-oxidant enzymes such as NADPH oxidases, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Epigenetic changes also have a key role in a similar way. Other mediators such as mammalian target of rapamycin (mTOR) and peroxisome proliferator-activated receptor (PPAR), which are involved in the normal metabolism of cells have also been shown to regulate cell death following exposure to radiation. These mechanisms are tissue specific. Inhibition or activation of each of these targets can be suggested for mitigation of radiation injury in a specific tissue. In the current paper, we review the cellular and molecular changes in the metabolism of cells and ROS/NO following exposure to radiation. Furthermore, the possible strategies for mitigation of radiation injury through modulation of cellular metabolism in irradiated organs will be discussed.

中文翻译：

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靶向细胞氧化还原代谢以减轻辐射损伤。

意外暴露于电离辐射是人类生活中的严重问题。减轻意外辐射事件后的副作用的研究正在进行中。最近的研究表明，辐射可以激活几种信号传导途径，从而导致自由基的代谢变化，包括活性氧（ROS）和一氧化氮（NO）。细胞和分子机制表明，辐射会破坏正常的还原/氧化（氧化还原）系统。暴露于辐射后的线粒体功能异常和线粒体DNA（mtDNA）的突变在慢性氧化应激中起关键作用。此外，暴露于辐射导致炎性细胞如巨噬细胞，淋巴细胞和肥大细胞的浸润，它们是ROS和NO的重要来源。这些细胞通过上调某些促氧化剂酶（例如NADPH氧化酶，诱导型一氧化氮合酶（iNOS）和环氧合酶2（COX-2））产生自由基。表观遗传的变化也以类似的方式起着关键作用。还显示参与细胞正常代谢的其他介质，例如雷帕霉素的哺乳动物靶标（mTOR）和过氧化物酶体增殖物激活的受体（PPAR），可调节暴露于辐射后的细胞死亡。这些机制是组织特异性的。可以建议抑制或激活这些靶标中的每一个，以减轻特定组织中的放射损伤。在当前的论文中，我们回顾了暴露于辐射后细胞代谢中的细胞和分子变化以及ROS / NO。此外，