3-Nitropropionic acid neurotoxicity is attenuated in copper/zinc superoxide dismutase transgenic mice.

摘要: The mitochondrial toxin 3-nitropropionic acid (3-NP) produces selective striatal lesions in both experimental animals and humans. pathogenesis of the involves secondary excitotoxicity that may then lead to free radical generation. To test this further we examined effects 3-NP transgenic (Tg) mice carry complete sequence for human copper/zinc superoxide dismutase (SOD) gene as well non-Tg littermate controls. Tg-SOD showed a pronounced attenuation Nissl-stained compared with mice. Systemic administration resulted production hydroxyl radicals assessed by conversion salicylate 2,3- 2,5-dihydroxybenzoic acid. This was attenuated significantly In similar way, produced significant increases 3-nitrotyrosine/tyrosine, marker peroxynitrite-mediated damage, which were These results support oxygen peroxynitrite play an important role neurotoxicity.