Russ Eric, Davis Catherine M, Slaven John E, Bradfield Dmitry T, Selwyn Reed G, Day Regina M
Graduate Program of Cellular and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Department of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Toxics. 2022 Oct 21;10(10):628. doi: 10.3390/toxics10100628.
Exposure to ionizing radiation can occur during medical treatments, from naturally occurring sources in the environment, or as the result of a nuclear accident or thermonuclear war. The severity of cellular damage from ionizing radiation exposure is dependent upon a number of factors including the absorbed radiation dose of the exposure (energy absorbed per unit mass of the exposure), dose rate, area and volume of tissue exposed, type of radiation (e.g., X-rays, high-energy gamma rays, protons, or neutrons) and linear energy transfer. While the dose, the dose rate, and dose distribution in tissue are aspects of a radiation exposure that can be varied experimentally or in medical treatments, the LET and eV are inherent characteristics of the type of radiation. High-LET radiation deposits a higher concentration of energy in a shorter distance when traversing tissue compared with low-LET radiation. The different biological effects of high and low LET with similar energies have been documented in vivo in animal models and in cultured cells. High-LET results in intense macromolecular damage and more cell death. Findings indicate that while both low- and high-LET radiation activate non-homologous end-joining DNA repair activity, efficient repair of high-LET radiation requires the homologous recombination repair pathway. Low- and high-LET radiation activate p53 transcription factor activity in most cells, but high LET activates NF-kB transcription factor at lower radiation doses than low-LET radiation. Here we review the development, uses, and current understanding of the cellular effects of low- and high-LET radiation exposure.
在医疗治疗过程中、环境中的天然来源或核事故或热核战争的情况下，都可能接触到电离辐射。电离辐射暴露对细胞造成损害的严重程度取决于多种因素，包括暴露的吸收辐射剂量（每单位质量暴露吸收的能量）、剂量率、暴露组织的面积和体积、辐射类型（例如X射线、高能伽马射线、质子或中子）以及线能量传递。虽然剂量、剂量率和组织中的剂量分布是辐射暴露的一些方面，可以在实验或医疗治疗中进行变化，但线能量传递和电子伏特是辐射类型的固有特征。与低线能量传递辐射相比，高线能量传递辐射在穿过组织时在更短的距离内沉积更高浓度的能量。高能和低能但线能量传递相似的辐射在动物模型体内和培养细胞中产生的不同生物学效应已有记录。高线能量传递会导致强烈的大分子损伤和更多细胞死亡。研究结果表明，虽然低线能量传递和高线能量传递辐射都会激活非同源末端连接DNA修复活性，但高线能量传递辐射的有效修复需要同源重组修复途径。低线能量传递和高线能量传递辐射在大多数细胞中都会激活p53转录因子活性，但高线能量传递在比低线能量传递辐射更低的辐射剂量下激活NF-κB转录因子。在这里，我们综述了低线能量传递和高线能量传递辐射暴露对细胞影响的发展、用途和当前认识。
