Hirata H, Cadet J L
NIH/NIDA, Division of Intramural Research, Baltimore, MD 21224, USA.
Brain Res Mol Brain Res. 1997 Aug;48(1):145-8. doi: 10.1016/s0169-328x(97)00121-6.
Peripheral administration of kainic acid (KA) can cause cell death in the hippocampus of rodents. This is thought to involve oxidative stress. In the present study, we tested the possibility that KA-induced neuronal cell death might be attenuated in CuZn superoxide dismutase transgenic (SOD-Tg) mice. Acute administration of KA causes animal death in a dose-dependent fashion; this was attenuated in SOD-Tg mice. Similarly, KA caused dose-dependent neuronal cell death in the hippocampus of wild-type mice; this cell death was attenuated in the SOD-Tg mice, in a gene-dosage-dependent fashion, with homozygous mice showing complete protection even at the highest dose (45 mg/kg) of KA used in this study. These results provide further support for the involvement of oxygen-based radicals in the toxic effects of KA.
向啮齿动物外周注射红藻氨酸（KA）可导致其海马体中的细胞死亡。这被认为与氧化应激有关。在本研究中，我们测试了在铜锌超氧化物歧化酶转基因（SOD-Tg）小鼠中，KA诱导的神经元细胞死亡可能会减轻的可能性。急性注射KA会以剂量依赖的方式导致动物死亡；而在SOD-Tg小鼠中这种情况有所减轻。同样，KA在野生型小鼠的海马体中会导致剂量依赖性的神经元细胞死亡；这种细胞死亡在SOD-Tg小鼠中以基因剂量依赖的方式减轻，纯合小鼠即使在本研究中使用的最高剂量（45毫克/千克）的KA作用下也表现出完全的保护作用。这些结果进一步支持了氧自由基参与KA毒性作用的观点。
