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NF-kappaB DNA-binding activity after high peak power pulsed microwave (8.2 GHz) exposure of normal human monocytes.
Bioelectromagnetics ( IF 1.8 ) Pub Date : 2002-04-12 , DOI: 10.1002/bem.10018
Mohan Natarajan 1 , Vijayalaxmi , Maria Szilagyi , Francis N Roldan , Martin L Meltz
Affiliation  

The hypothesis investigated is that exposure of a mammalian cell to high peak power pulsed RF, at the frequency of 8.2 GHz, can result in the activation of an important eukaryotic transcriptional regulator, nuclear factor kappa B (NF-kappaB). This DNA-binding protein controls genes involved in long term cellular regulation. The selection of 8.2 GHz was based on the availability of a high peak power pulsed RF transmitter. In these studies, triplicate cultures of human monocytes (Mono Mac-6) were exposed to the pulsed wave radiation. The peak to average power ratio was 455:1 (2.2 micros pulse width and pulse repetition rate of 1000 pulses/s). The average power density at the position of exposure was 50 W/m(2), and the mean SAR at the bottom of the culture flask was 10.8 +/- 7.1 W/kg. The FDTD analysis indicated that 10% of the cells had an SAR of 22-29 W/kg. The cells were exposed continuously for 90 min at 37 degrees C, reincubated at this temperature, and harvested 4 h postexposure. The nuclear extracts were analyzed by electrophoretic mobility shift assay. The results showed a profound increase (3.6-fold) in the DNA binding activity of NF-kappaB in monocytes at 4 h after the pulsed RF exposure compared to sham irradiated controls. Competition experiments with cold NF-kappaB- specific oligonucleotides confirmed the specificity of the DNA binding activity. These results provide evidence that high peak power pulsed radiofrequency radiation can perturb the cell and initiate cell signaling pathways. However, at this point, we are not prepared to advocate that the cause is a nonthermal mechanism. Because of the broad distribution of SAR's in the flask, experiments need to be performed to determine if the changes observed are associated with cells exposed to high or low SARs.

中文翻译:

正常人单核细胞在高峰值功率脉冲微波(8.2 GHz)照射后的NF-κBDNA结合活性。

所研究的假设是,哺乳动物细胞在8.2 GHz频率下暴露于高峰值功率脉冲RF中会导致重要的真核转录调节因子核因子κB(NF-κB)激活。这种DNA结合蛋白控制着涉及长期细胞调节的基因。8.2 GHz的选择基于高峰值功率脉冲RF发射机的可用性。在这些研究中,人类单核细胞(Mono Mac-6)的三次重复培养暴露于脉冲波辐射下。峰均功率比为455:1(2.2微米脉冲宽度和1000脉冲/秒的脉冲重复率)。暴露位置的平均功率密度为50 W / m(2),培养瓶底部的平均SAR为10.8 +/- 7.1 W / kg。FDTD分析表明,10%的细胞的SAR为22-29 W / kg。将细胞在37摄氏度下连续暴露90分钟,在此温度下重新孵育,并在暴露后4小时收获。通过电泳迁移率变动分析法分析核提取物。结果显示,与假照射的对照组相比,脉冲RF暴露后4 h,单核细胞中NF-κB的DNA结合活性显着增加(3.6倍)。用冷的NF-κB特异性寡核苷酸进行的竞争实验证实了DNA结合活性的特异性。这些结果提供了高峰值功率脉冲射频辐射可以扰动细胞并启动细胞信号通路的证据。但是,在这一点上,我们还没有准备好主张原因是非热机制。
更新日期:2019-11-01
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