Study of Pathogenic Mechanism of Oxidative Stress by Vitamin B12 Deficiency using Caenorhabditis elegans
| Project/Area Number |
17K15270
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Food science
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| Research Institution | Tottori University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ビタミンB12 / 酸化ストレス / 線虫 / Caenorhabditis elegans / 抗酸化物質 / 寿命 / 体内リズム / レドックス制御 / 老化 |
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| Outline of Final Research Achievements |
To clarify the mechanism of vitamin B12 (B12)-deficient neuropathy that occurs frequently in elderly people, this study focused on the mechanism of oxidative stress disorder induced by B12 deficiency. Analysis using the model organism C. elegans revealed that B12 deficiency results in significant decrease in gene expression and enzyme activity of some antioxidant enzymes. From these results, it was inferred that the failure of antioxidant system is the cause of leading severe oxidative stress in B12 deficiency. In addition, as the results of studying the relationship between B12 deficiency and lifespan or aging, it became clear that a specific clock gene shows remarkable expression fluctuation.
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| Academic Significance and Societal Importance of the Research Achievements |
ビタミンB12(B12)欠乏症で誘発される酸化ストレス障害は抗酸化システムが破綻することで生じることが推察された。酸化ストレスと神経疾患の関連性が数多く報告されていることから、B12欠乏性神経障害の要因としてB12欠乏で誘導される酸化ストレスが一因であることが挙げられ、その発症機構を部分的に解いたことの学術的意義は大きい。またB12欠乏症の酸化ストレスは抗酸化物質(グルタチオンやビタミンC)を供給することで解消されるが、この結果はB12欠乏症において多量の抗酸化物質を摂取することは、真のB12欠乏症の症状を覆い隠すことに繋がる。医療現場等において非常に重要な知見である。
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Report
(3 results)
Research Products
(6 results)
