Toxicological mechanism of oxidative stress-induced motoneuron death in the neurolathyrism rat model
| Project/Area Number |
22590088
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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 |
Biological pharmacy
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| Research Institution | Nihon University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 神経生物学 / 疾患モデル / 運動神経疾患 / ニューロラチリズム / カルシウムイオン / 酸化ストレス / TRPチャネル / ヘムオキシゲナーゼ１ / 血管 / 脊髄 / 運動神経 / 運動疾患 / 血管障害 / 神経毒 / 毒性学 |
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| Research Abstract |
Neurolathyrism (NL), a motoneuron disease, is caused by the overconsumption of grass pea that is a draught-tolerant crop containing a neurotoxin L-β-ODAP. Under the unavoidable deficiencies of sulfur-containing amino acids and glutathione, I clarified the induction of nonspecific cation channels TRPM2 and 7 in cultured cells and in the spinal cord of a NL-model rat. In the model, there observed the vessel disruption and hemorrhage in the lower spinal cord where heme oxygenase-1 was highly induced to cause pathological changes.
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Report
(4 results)
Research Products
(26 results)
