Suppression of high-density magnetic field (400 mT at 50 Hz)-induced mutations by wild-type p53 expression in human osteosarcoma cells.-猫眼课题宝

通过在人骨肉瘤细胞中表达野生型 p53 来抑制高密度磁场（400 mT，50 Hz）诱导的突变。

DOI：

10.1006/bbrc.1997.8140

发表时间：

1998

期刊：

Biochemical and biophysical research communications

影响因子：

3.1

通讯作者：

中科院分区：

生物学4区

文献类型：

作者：

J. Miyakoshi;Y. Mori;N. Yamagishi;K. Yagi;H. Takebe

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）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），所述Saos-LP-12细胞分离自亲本Saos-2细胞并且在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（+）]和假暴露处理之间未观察到突变谱的显著差异。我们的研究结果表明，野生型p53具有抑制DNA复制错误和/或在高密度ELFMF暴露后维持基因组稳定性的功能。

Exposure of cultured human osteosarcoma cells (Saos-LP-12) to high-density (400 mT at 50 Hz) extremely low frequency magnetic fields (ELFMF) induced mutations in the hypoxanthine-guanine phosphoribosyl transferase gene. Saos-LP-12 cells, which are isolated from 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 400 mT 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.