Pellegrini-Giampietro D E, Cherici G, Alesiani M, Carlà V, Moroni F
Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, University of Florence, Italy.
J Neurochem. 1988 Dec;51(6):1960-3. doi: 10.1111/j.1471-4159.1988.tb01187.x.
The release of D-[3H]aspartate, [3H]noradrenaline, and of endogenous glutamate and aspartate from rat hippocampal slices was significantly increased when the slices were incubated with xanthine oxidase plus xanthine to produce superoxide and hydroxyl free radicals locally. Allopurinol, a specific xanthine oxidase inhibitor, the hydroxyl-radical scavenger D-mannitol, or the superoxide-radical scavenger system formed by superoxide dismutase plus catalase prevented this release. These results suggest that endogenous excitatory amino acids are released consequent to the formation of free radicals. The excess of glutamate and aspartate released by this mechanism could be one of the factors contributing to the death of neurons after anoxic or ischemic injuries.
当大鼠海马切片与黄嘌呤氧化酶加黄嘌呤一起孵育以在局部产生超氧化物和羟基自由基时，D-[3H]天冬氨酸、[3H]去甲肾上腺素以及内源性谷氨酸和天冬氨酸的释放显著增加。黄嘌呤氧化酶特异性抑制剂别嘌呤醇、羟基自由基清除剂D-甘露醇或由超氧化物歧化酶加过氧化氢酶形成的超氧化物自由基清除剂系统可阻止这种释放。这些结果表明，自由基形成后会导致内源性兴奋性氨基酸释放。由此机制释放的过量谷氨酸和天冬氨酸可能是导致缺氧或缺血性损伤后神经元死亡的因素之一。
