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暴露于900MHz射频场的HL-60细胞中的线粒体DNA损伤和氧化损伤。

Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz radiofrequency fields.

作者信息

Sun Yulong, Zong Lin, Gao Zhen, Zhu Shunxing, Tong Jian, Cao Yi

机构信息

School of Public Health, Soochow University, Suzhou, Jiangsu Province, PR China.

Laboratory Animal Center, Nantong University, Nantong, Jiangsu Province, PR China.

出版信息

Mutat Res. 2017 Mar;797-799:7-14. doi: 10.1016/j.mrfmmm.2017.03.001. Epub 2017 Mar 7.

DOI:10.1016/j.mrfmmm.2017.03.001
PMID:28340409
Abstract

HL-60 cells, derived from human promyelocytic leukemia, were exposed to continuous wave 900MHz radiofrequency fields (RF) at 120μW/cm power intensity for 4h/day for 5 consecutive days to examine whether such exposure is capable damaging the mitochondrial DNA (mtDNA) mediated through the production of reactive oxygen species (ROS). In addition, the effect of RF exposure was examined on 8-hydroxy-2'-dexoyguanosine (8-OHdG) which is a biomarker for oxidative damage and on the mitochondrial synthesis of adenosine triphosphate (ATP) which is the energy required for cellular functions. The results indicated a significant increase in ROS and significant decreases in mitochondrial transcription factor A, mtDNA polymerase gamma, mtDNA transcripts and mtDNA copy number in RF-exposed cells compared with those in sham-exposed control cells. In addition, there was a significant increase in 8-OHdG and a significant decrease in ATP in RF-exposed cells. The response in positive control cells exposed to gamma radiation (GR, which is also known to induce ROS) was similar to those in RF-exposed cells. Thus, the overall data indicated that RF exposure was capable of inducing mtDNA damage mediated through ROS pathway which also induced oxidative damage. Prior-treatment of RF- and GR-exposed the cells with melatonin, a well-known free radical scavenger, reversed the effects observed in RF-exposed cells.

摘要

源自人早幼粒细胞白血病的HL-60细胞,以120μW/cm的功率强度暴露于连续波900MHz射频场(RF)中,每天暴露4小时,连续暴露5天,以检查这种暴露是否能够通过产生活性氧(ROS)介导损伤线粒体DNA(mtDNA)。此外,还研究了RF暴露对作为氧化损伤生物标志物的8-羟基-2'-脱氧鸟苷(8-OHdG)以及对细胞功能所需能量三磷酸腺苷(ATP)的线粒体合成的影响。结果表明,与假暴露对照细胞相比,RF暴露细胞中的ROS显著增加,线粒体转录因子A、mtDNA聚合酶γ、mtDNA转录本和mtDNA拷贝数显著减少。此外,RF暴露细胞中的8-OHdG显著增加,ATP显著减少。暴露于γ辐射(GR,已知也可诱导ROS)的阳性对照细胞中的反应与RF暴露细胞中的反应相似。因此,总体数据表明,RF暴露能够诱导通过ROS途径介导的mtDNA损伤,这也会诱导氧化损伤。用褪黑素(一种著名的自由基清除剂)对RF和GR暴露的细胞进行预处理,可逆转在RF暴露细胞中观察到的效应。

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