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Cellular and molecular mechanisms of magnetic fields

磁场的细胞和分子机制

基本信息

批准号：
10837006
负责人：
MIYAKOSHI Junji
金额：
$ 2.43万
依托单位：
KYOTO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

Exposure of cultured human ostosarcoma cells (Saos-LP-12) to high-density (400mT at 50Hz) extremely low frequency magnetic fields (ELFMF) induced mutations in the hypoxanthine-guanine phosphoribosyl transferase gene. Saos-LP-12 cells, which are isolated form parental Saos-2 cells and have a deletion in the coding region of the p53 gene, are introduced to the wild-type (wt) p53 expression plasmid (pOPRSVp53). The mutation in Saos-LP-12 cells was suppressed by expression of the introduced wt p53 gene during 400mT ELFMF exposure. No. marked difference in the mutation spectrum was observed among the treatments of ELFMF [p53(-)], ELFMF [P53(+)], and sham exposures. Our findings suggest that wt p53 has a function in suppression of DNA replication errors and/or in maintenance of genomic stability after high-density ELFMF exposure.On the other hand, enhanced expression of neuron derived orphan receptor (NOR-1) gene was observed by exposure of Chinese hamster ovary K1 (CHO-K1) cells to ELFMF of 50Hz at 400mT, but not at 5mT. The enhanced expression, reaching the maximum at 6h, was transient and reduced to the control level after exposure to 400mT ELFMF for 24h. The NOR-1 expression induced by treatment with forskolin and TPA was further enhanced by the simultaneous treatment with 400mT ELFMF, in which the maximum response was at 3h. The NOR-1 expression by these treatments was induced more earlier than that by 400mT ELFMF alone. When cells were treated with an inhibitor of the protein kinase C (calphostin C or crocetin) and CaィイD12+ィエD1 entry blockers (nifedipin and dantrolen) during the 400mT ELFMF exposure, the enhanced NOR-1 expression was not observed. Exposure of CHO-K1 cells to the high-density 400mT ELFMF may affect the signal transduction in the cells, resulting in the enhanced NOR-1 gene expression.

将培养的人骨肉瘤细胞（Saos-LP-12）暴露于高密度（400 mT，50 Hz）极低频磁场（ELFMF）中，诱导次黄嘌呤-鸟嘌呤磷酸核糖转移酶基因突变。将Saos-LP-12细胞导入野生型（wt）p53表达质粒（pOPRSVp 53）中，所述Saos-LP-12细胞是从亲本Saos-2细胞中分离的并且在p53基因的编码区中具有缺失。在400 mT ELFMF暴露期间，Saos-LP-12细胞中的突变被引入的wt p53基因的表达抑制。在ELFMF [P53（-）]、ELFMF [P53（+）]和假暴露处理之间观察到突变谱的显著差异。结果表明，野生型p53在高密度ELFMF作用下具有抑制DNA复制错误和/或维持基因组稳定性的功能，而在50 Hz、400 mT的ELFMF作用下，中国仓鼠卵巢K1（CHO-K1）细胞的神经元源孤儿受体（NOR-1）基因表达增强，而在5 mT的ELFMF作用下则无此作用。400 mT ELFMF作用24 h后，表达水平下降至对照组水平。同时用400 mT ELFMF处理后，forskolin和TPA诱导的NOR-1表达进一步增强，最大反应出现在3 h。这些处理诱导NOR-1的表达比单独400 mT ELFMF诱导更早。当细胞在400 mT ELFMF暴露期间用蛋白激酶C抑制剂（calphostin C或藏红花酸）和Ca ~（2+）D12+ Ca ~（2+）D1进入阻断剂（硝苯地平和丹曲伦）处理时，未观察到NOR-1表达的增强。CHO-K1细胞暴露于高密度400 mT ELFMF可能影响细胞内的信号转导，导致NOR-1基因表达增强。