2012 Fiscal Year Final Research Report
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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| Keywords | 神経生物学 / 疾患モデル |
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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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