| Project/Area Number |
15H06174
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2015-08-28 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | MnSOD / SOD2 / 騒音性難聴 / 酸化ストレス / ミトコンドリア / ＭｎＳＯＤ / ＳＯＤ２ |
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| Outline of Final Research Achievements |
Manganese superoxide dismutase (MnSOD) is one of the antioxidant enzymes acting within the mitochondria. To investigate the pathological role of mitochondrial antioxidant stress in the cochlea, we generated systemic MnSOD heterozygous knockout (Sod2+/-) mice, and investigated hearing loss and histological damage after noise exposure.
The mean thresholds of auditory brainstem responses were significantly worse in the Sod2+/- group on post-noise days 7 and 14. Histologically, compared with control group, outer hair cell survival rate in the Sod2+/- group was significantly decreased in all cochlear turns.
We showed that delay of hearing recovery and outer hair cell damage occur after noise exposure with decreasing MnSOD. These findings suggest that MnSOD has important role to reduce reactive oxygen species in hair cell, thereby protecting from noise induced hearing loss.
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