Department of Biophysics, Yozgat Bozok University, Medical School, Yozgat, Turkey.
Department of Biotechnology, Biotechnology Institute, Ankara University, Ankara, Turkey.
Electromagn Biol Med. 2022 Oct 2;41(4):389-401. doi: 10.1080/15368378.2022.2117187. Epub 2022 Sep 5.
This study aims to determine whether exposure to non-ionizing radiofrequency fields could induce an adaptive response (AR) in adult mice and to reveal potential molecular mechanisms triggered by RF-induced AR. The study was performed on 24 adult male Swiss-Albino mice. The average mass of the mice was 37 g. Four groups of adult mice, each consisting of 6, were formed. The radiofrequency group (R) and the adaptive response group (RB) were exposed to 900 MHz of global system for mobile communications (GSM) signal at 0.339 W/kg (1 g average specific absorption rate) 4 h/day for 7 days, while the control group (C) and the bleomycin group (B) were not exposed. 20 minutes after the last radiofrequency field (RF) exposure, the mice in the B and RB groups were injected intraperitoneal (ip) bleomycin (BLM), 37.5 mg/kg. All the animals were sacrificed 30 minutes after the BLM injection. Oxidative damage and antioxidant mechanism were subsequently investigated in the blood samples. Changes in the expression of the genes involved in DNA repair were detected in the liver tissue. TUNEL method was used to determine the apoptosis developed by DNA fragmentation in the liver tissue. The RB group, which produced an adaptive response, was compared with the control group. According to the results, the increase of reactive oxygen species (ROS) in the RB group may have played an important role in triggering the adaptive response and producing the required minimum stress level. Furthermore, tumor suppressor 53(p53), oxo guanine DNA glycosylase (OGG-1) levels responsible for DNA repair mechanism genes expression were increased in conjunction with the increase in ROS. The change in the poly (ADP-ribose) polymerase 1 (PARP-1) and glutathione peroxidase 1 (GPx-1) gene expression were not statistically significant. The antioxidant enzyme levels of superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC) were decreased in the group with adaptive response. According to the data obtained from terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis, apoptosis was decreased in the RB group due to the decrease in cell death, which might have resulted from an increase in gene expression responsible for DNA repair mechanisms. The results of our study show that exposure to RF radiation may create a protective reaction against the bleomycin. The minimal oxidative stress due to the RF exposure leads to an adaptive response in the genes that play a role in the DNA repair mechanism and enzymes, enabling the survival of the cell.
这项研究旨在确定非电离射频场暴露是否会引起成年小鼠的适应性反应（AR），并揭示射频诱导 AR 所触发的潜在分子机制。研究对象为 24 只成年雄性瑞士白化小鼠。小鼠的平均体重为 37g。形成了四组成年小鼠，每组 6 只。射频组（R）和适应性反应组（RB）暴露于 900MHz 的全球移动通信系统（GSM）信号下，强度为 0.339W/kg（1g 平均比吸收率），每天 4 小时，持续 7 天，而对照组（C）和博来霉素组（B）则不暴露于射频。最后一次射频场（RF）暴露后 20 分钟，B 组和 RB 组的小鼠经腹腔内（ip）注射博来霉素（BLM），剂量为 37.5mg/kg。BLM 注射后 30 分钟，所有动物均被处死。随后在血液样本中研究了氧化损伤和抗氧化机制，在肝组织中检测了参与 DNA 修复的基因的表达变化。采用 TUNEL 法检测肝组织中因 DNA 片段化而导致的细胞凋亡。将产生适应性反应的 RB 组与对照组进行比较。结果表明，RB 组中活性氧（ROS）的增加可能在触发适应性反应和产生所需的最低应激水平方面发挥了重要作用。此外，负责 DNA 修复机制基因表达的肿瘤抑制因子 53（p53）、氧化鸟嘌呤 DNA 糖基化酶（OGG-1）水平也随着 ROS 的增加而增加。多聚（ADP-核糖）聚合酶 1（PARP-1）和谷胱甘肽过氧化物酶 1（GPx-1）基因表达的变化无统计学意义。超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和总抗氧化能力（TAC）等抗氧化酶水平在具有适应性反应的组中降低。根据末端脱氧核苷酸转移酶 dUTP 缺口末端标记（TUNEL）分析获得的数据，由于细胞死亡减少，RB 组中的细胞凋亡减少，这可能是由于负责 DNA 修复机制的基因表达增加所致。我们的研究结果表明，射频辐射暴露可能会对博来霉素产生保护反应。射频暴露引起的最小氧化应激导致 DNA 修复机制和酶中发挥作用的基因产生适应性反应，使细胞得以存活。
