| Project/Area Number |
23592570
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Shimane University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANITO Masaki 島根大学, 医学部, 講師 (30284037)
KAIDZU Sachiko 島根大学, 医学部, 助教 (00325052)
NAKABEPPU Yusaku 九州大学, 生体防御医学研究所, 教授 (30180350)
OKUNO Tsutomu 労働安全衛生研究所, 人間工学・リスク研究グループ, 部長 (90332395)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 酸化ストレス / OGG1 / MUTYH / MTH1 / 網膜光障害 / OGG１ / MUTHY |
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| Research Abstract |
The present study aimed to elucidate the pathological mechanism in light induced retinal damage using 8-oxoguanine-DNA glycosylase (OGG1), human MutT Homolog 1 (MTH1) and MutY glycosylase homologue (MUTYH) knockout mice. Mice were exposed to 350-385 nm wavelengths light, and retinal radiant exposure was 75 J/cm2. Retinal light damage was reduced in MUTYH knockout mice, indicating that MUTYH involved in the pathological mechanism of light damage. Our results show the possibility that the suppression of neurodegeneration by control of MUTYH may effectively protect retinal light damage.
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