1999 Fiscal Year Final Research Report Summary
Cellular and molecular mechanisms of magnetic fields
| Project/Area Number |
10837006
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
電磁場環境
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
MIYAKOSHI Junji GRADUATE SCHOOL OF MEDICINE, KYOTO UNIVERSITY ASSOCIATE PROFESSOR, 医学研究科, 助教授 (70121572)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMORI Akira GRADUATE SCHOOL OF MEDICINE, KYOTO UNIVERSITY RESEARCH ASSOCIATE, 医学研究科, 助手 (50314183)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Magnetic fields / Mutation induction / Mutation spectrum / Gene expression / NOR-1 / Signal transduction |
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| Research Abstract |
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.
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