He Qina, Zong Lin, Sun Yulong, Prihoda Thomas J, Tong Jian, Cao Yi
School of Public Health, Medical College of Soochow University, Suzhou Jiangsu Province, People's Republic of China.
Deparment of Radiology, University of Texas Health Science Center, San Antonio, TX, USA.
Mutat Res Genet Toxicol Environ Mutagen. 2017 Aug;820:19-25. doi: 10.1016/j.mrgentox.2017.05.007. Epub 2017 May 17.
This study examined whether non-ionizing radiofrequency fields (RF) exposure is capable of inducing poly (ADP-ribose) polymerase-1 (PARP-1) in bone marrow stromal cells (BMSCs) and whether it plays a role in RF-induced adaptive response (AR). Bone marrow stromal cells (BMSCs) were exposed to 900MHz RF at 120μW/cm power flux density for 3h/day for 5days and then challenged with a genotoxic dose of 1.5Gy gamma-radiation (GR). Some cells were also treated with 3-aminobenzamide (3-AB, 2mM final concentration), a potent inhibitor of PARP-1. Un-exposed and sham (SH)-exposed control cells as well as positive control cells exposed to gamma radiation (GR) were included in the experiments. The expression of PARP-1 mRNA and its protein levels as well as single strand breaks in the DNA and the kinetics of their repair were evaluated at several times after exposures. The results indicated the following. (a) Cells exposed to RF alone showed significantly increased PARP-1 mRNA expression and its protein levels compared with those exposed to SH- and GR alone. (b) Treatment of RF-exposed cells with 3-AB had diminished such increase in PARP-1. (c) Cells exposed to RF+GR showed significantly decreased genetic damage as well as faster kinetics of repair compared with those exposed to GR alone. (d) Cells exposed to RF+3-AB+GR showed no such decrease in genetic damage. Thus, the overall date suggested that non-ionizing RF exposure was capable of inducing PARP-1 which has a role in RF-induced AR.
本研究检测了非电离射频场（RF）暴露是否能够诱导骨髓基质细胞（BMSC）中的聚（ADP-核糖）聚合酶-1（PARP-1），以及它是否在射频诱导的适应性反应（AR）中发挥作用。将骨髓基质细胞（BMSC）暴露于功率通量密度为120μW/cm的900MHz射频下，每天暴露3小时，共暴露5天，然后用1.5Gy的遗传毒性剂量的γ射线（GR）进行攻击。一些细胞还用PARP-1的强效抑制剂3-氨基苯甲酰胺（3-AB，终浓度为2mM）进行处理。实验中包括未暴露和假暴露（SH）的对照细胞以及暴露于γ射线（GR）的阳性对照细胞。在暴露后的几个时间点评估PARP-1 mRNA的表达及其蛋白水平，以及DNA中的单链断裂及其修复动力学。结果如下所示。（a）与单独暴露于SH和GR的细胞相比，单独暴露于RF的细胞显示PARP-1 mRNA表达及其蛋白水平显著增加。（b）用3-AB处理RF暴露的细胞可减少PARP-1的这种增加。（c）与单独暴露于GR的细胞相比，暴露于RF+GR的细胞显示遗传损伤显著减少，并且修复动力学更快。（d）暴露于RF+3-AB+GR的细胞在遗传损伤方面没有这种减少。因此，总体数据表明，非电离RF暴露能够诱导PARP-1，其在RF诱导的AR中发挥作用。
