Toxicological mechanism of oxidative stress-induced motoneuron death in the neurolathyrism rat model

神经性甲状腺肿(NL)是一种运动神经元疾病，是由过量食用草豆引起的，草豆是一种含有神经毒素L-β-ODAP的耐旱作物。在含硫氨基酸和谷胱甘肽不可避免地缺乏的情况下，我阐明了培养细胞和NL模型大鼠脊髓中非特异性阳离子通道TRPM2和7的诱导。在模型中，观察到下段脊髓血管破裂和出血，其中血红素加氧酶-1被高度诱导而引起病变。

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.