Increase in X-ray-induced mutations by exposure to magnetic field (60 Hz, 5 mT) in NF-κB-inhibited cells
Increase in X-ray-induced mutations by exposure to magnetic field (60 Hz, 5 mT) in NF-κB-inhibited cells
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DOI：
10.1006/bbrc.2000.3455
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发表时间：
2000-09-16
影响因子：
3.1
通讯作者：
Miyakoshi, J
中科院分区：
文献类型：
--
作者：
Ding, GR;Yaguchi, H;Miyakoshi, J
它是建立极低频磁场（ELFMF）的磁通密度，即，5 mT及以下，无致突变性。然而，暴露于ELFMF增强了X射线诱导的突变。在这项研究中，我们研究了长期暴露于5 mT ELFMF对具有不同突变I κ B-α（NF-κ B的关键抑制剂）基因的人恶性胶质瘤细胞（MO 54）的突变诱导和X射线诱导突变的影响。将细胞暴露于或假暴露于5 mT ELFMF中长达8天，有或没有初始X射线（4戈伊），并分析次黄嘌呤-鸟嘌呤磷酸核糖转移酶（HPRT）基因的突变频率。ELFMF联合X射线照射后，与单独使用丝氨酸突变型I κ B α基因或载体相比，使用酪氨酸突变型I κ B α基因的MO 54细胞，X射线诱导的突变明显增加。ELFMF单独作用可显著增加MO 54-V细胞中I κ B-α基因的突变率，并可增加X射线诱导的MO 54-V细胞的凋亡率，而磁场对MO 54-SY 4细胞有抗凋亡作用。我们的数据表明，暴露于5 mT ELFMF可能会诱导突变和增强X射线诱导的突变，导致NF-κ B B通过抑制酪氨酸磷酸化的失活。(C)北京大学出版社.
It is established that extremely low frequency magnetic fields (ELFMF) at the flux densities, i.e., 5 mT and less, are not mutagenic. However, exposure to ELFMF enhances mutations induced by X-rays. In this study, we examined the effects of long-term exposure to 5 mT ELFMF on mutation induction and X-ray-induced mutations in human malignant glioma cells (MO54) with different mutant I kappa B-alpha (a critical inhibitor of NF-kappa B) genes. Cells were exposed or sham-exposed to 5 mT ELFMF for up to 8 days with or without initial X-rays (4 Gy), and the mutant frequency of hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene was analyzed. An obvious increase in X-ray-induced mutations was observed after treatment with ELFMF in combination with X-irradiation in MO54 cells with tyrosine mutant I kappa B-alpha gene other than with serine mutant I kappa B-alpha gene or vector alone. Exposure to ELFMF alone increased mutations significantly in MO54 cells with tyrosine mutant I kappa B-alpha gene, In addition, X-ray-induced apoptoic cells were increased in MO54-V cells after exposure to ELFMF, while an anti-apoptotic effect of magnetic field was found in MO54-SY4 cells. Our data suggest that exposure to 5 mT ELFMF may induce mutations and enhance X-ray-induced mutations, resulting from the inactivation of NF-kappa B through the inhibition of tyrosine phosphorylation. (C) 2000 Academic Press.