The duration of exposure to 50 Hz magnetic fields: Influence on circadian genes and DNA damage responses in murine hematopoietic FDC-P1 cells

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Ehab Mustafa , Jukka Luukkonen , Jenny Makkonen , Jonne Naarala
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引用次数: 3

Abstract

We investigated the effects of 50 Hz extremely low-frequency magnetic fields (MFs) on gene expression related to the circadian rhythm or DNA damage signaling and whether these fields modify DNA damage repair rate after bleomycin treatment. Murine FDC-P1 hematopoietic cells were exposed for different durations (15 min, 2 h, 12 h, and 24 h) to either 200 μT MFs or sham-exposures. Cells were then collected for comet assay or real-time PCR to determine immediate DNA damage level and circadian rhythm gene expression, respectively. To assess DNA-damage signaling and DNA repair rate, the cells were subsequently treated with 20 μg/mL bleomycin for 1 h and then either assayed immediately or allowed to repair their DNA for 1 or 2 h. We found that circadian rhythm-related genes were upregulated after 12 h of MF exposure and downregulated after 24 h of MF exposure, but none of the affected genes were core genes controlling the circadian rhythm. In addition, we found that the repair rate for bleomycin-induced damage was only decreased after MF exposure for 24 h. In conclusion, our findings suggest that the effects of MFs are duration-dependent; they were observed predominantly after long exposures.

暴露于50hz磁场的持续时间:对小鼠造血FDC-P1细胞的昼夜节律基因和DNA损伤反应的影响
我们研究了50 Hz极低频磁场(MFs)对与昼夜节律或DNA损伤信号相关的基因表达的影响,以及这些磁场是否会改变博来霉素治疗后DNA损伤修复率。小鼠FDC-P1造血细胞分别暴露于200 μT MFs和假暴露中,暴露时间分别为15分钟、2小时、12小时和24小时。然后收集细胞进行彗星试验或实时PCR,分别测定即时DNA损伤水平和昼夜节律基因表达。为了评估DNA损伤信号传导和DNA修复率,细胞随后被20 μg/mL博来霉素处理1小时,然后立即检测或修复DNA 1或2小时。我们发现,与昼夜节律相关的基因在MF暴露12小时后上调,在MF暴露24小时后下调,但受影响的基因都不是控制昼夜节律的核心基因。此外,我们发现,在MF暴露24小时后,博莱霉素诱导的损伤修复率仅下降。总之,我们的研究结果表明,MF的作用是持续依赖的;它们主要是在长时间曝光后观察到的。
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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
审稿时长
51 days
期刊介绍: Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.
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