3-NITROPROPIONIC ACID INDUCES APOPTOSIS IN CULTURED STRIATAL AND CORTICAL-NEURONS
3-NITROPROPIONIC ACID INDUCES APOPTOSIS IN CULTURED STRIATAL AND CORTICAL-NEURONS
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DOI：
10.1097/00001756-199502000-00034
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发表时间：
1995-02-15
期刊：
影响因子：
1.7
通讯作者：
CHOI, DW
中科院分区：
文献类型：
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作者：
BEHRENS, MI;KOH, J;CHOI, DW
在发霉的甘蔗中摄入3-硝基丙酸（3-NPA）会导致儿童脑损伤。3-NPA毒性的机制被认为是抑制能量产生，导致ATP消耗和兴奋性毒性。我们将培养的小鼠纹状体或皮质神经元暴露于1-2 mM 3-NPA 48 h。这种暴露产生以细胞体收缩和DNA片段化为特征的逐渐神经元变性。在3-NPA暴露期间添加谷氨酸拮抗剂并没有减少神经元死亡。然而，添加大分子合成抑制剂放线菌酮，emphetrin或放线菌素D显着减少神经元死亡。我们的研究结果并不排除3-NPA可以诱导兴奋性毒性在更完整的系统，但提出了额外的可能性，3-NPA也可能采取行动，以诱导神经元凋亡。
INGESTION of 3-nitropropionic acid (3-NPA) in moldy sugar cane causes brain damage in children. The mechanism of 3-NPA toxicity is thought to be inhibition of energy production, leading to ATP depletion and excitotoxicity. We exposed cultured mouse striatal or cortical neurons to 1-2 mM 3-NPA for 48 h. This exposure produced gradual neuronal degeneration characterized by cell body shrinkage and DNA fragmentation. Addition of glutamate antagonists during 3-NPA exposure did not reduce neuronal death. However, addition of the macromolecular synthesis inhibitors cycloheximide, emetine or actinomycin D markedly reduced neuronal death. Our results do not exclude that 3-NPA can induce excitotoxicity in more intact systems, but raise the additional possibility that 3-NPA may also act to induce neuronal apoptosis.