| Project/Area Number |
25282015
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Clothing life/Dwelling life
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| Research Institution | National Institute of Public Health |
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Principal Investigator |
KUNUGITA Naoki 国立保健医療科学院, 生活環境研究部, 部長 (90178020)
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| Co-Investigator(Kenkyū-buntansha) |
Tin・Tin Win・Shwe 国立研究開発法人国立環境研究所, 環境健康研究センター, 主任研究員 (00391128)
USHIYAMA Akira 国立保健医療科学院, 生活環境研究部, 上席主任研究官 (60291118)
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| Co-Investigator(Renkei-kenkyūsha) |
OKAMURA Kazuyuki 国立研究開発法人国立環境研究所, 環境健康研究センター, 研究員 (50736064)
OHTANI Shin 明治薬科大学, 薬学部, 特任研究員 (70507483)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | 携帯電話 / 電磁界 / マウス / 中枢神経系 / 行動試験 / 中枢神経 |
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| Outline of Final Research Achievements |
Pregnant C57BL/6J mice were exposed to RF-EMF (2.14 GHz, SAR; 4W/kg, 0.4W/kg) for one hour per day from day 7 to 17. Some mice were exposed again to RF-EMF from postnatal week 4 to 8.
We found that inflammatory markers (TNF-alpha, COX2), apoptosis markers (Bcl2) and oxidative stress markers (HO-1) mRNA expressions in the hippocampus were increased significantly in mice exposed to RF-EMF during organogenesis and adolescent periods. Moreover, we also examined the memory function related genes NMDA receptor subunits (NR1, NR2A and NR2B) expressions in the hippocampus and we did not find any significant changes between the control and exposure groups. Regarding novel object recognition test, we found that RF-EMF exposure did not affect novel object discrimination ability in RF-EMF exposed mice. Our results show that RF-EMF exposure during both developmental periods may induce inflammatory response in brain via modulation of apoptotic gene and oxidative stress markers.
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