Increase in X-ray-induced mutations by exposure to magnetic field (60 Hz, 5 mT) in NF-κB-inhibited cells

被引:23
作者
Ding, GR
Yaguchi, H
Yoshida, M
Miyakoshi, J [1 ]
机构
[1] Fourth Mil Med Univ, Dept Radiat Med, Xian 710032, Peoples R China
[2] Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan
[3] Kyoto Univ, Grad Sch Human & Environm Studies, Sakyo Ku, Kyoto 6068501, Japan
基金
日本学术振兴会;
关键词
extremely low frequency magnetic field (ELFMF); MO54; cells; NF-kappa B; hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene; mutant frequency;
D O I
10.1006/bbrc.2000.3455
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:238 / 243
页数:6
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