Newcomer T A, Rosenberg P A, Aizenman E
Department of Neurobiology, University of Pittsburgh School of Medicine, Pennsylvania 15261.
J Neurochem. 1995 Apr;64(4):1742-8. doi: 10.1046/j.1471-4159.1995.64041742.x.
2,4,5-Trihydroxyphenylalanine (TOPA) oxidizes in solution to form a quinone derivative that is a non-NMDA glutamatergic agonist and neurotoxin. DOPA can autoxidize in physiological solutions to form small amounts of both TOPA and TOPA quinone. We report here that this conversion can be dramatically enhanced by iron (II) alone, but more so by iron (II) in the presence of hydrogen peroxide. This conversion is of sufficient magnitude that the resulting product can elicit non-NMDA, glutamate receptor-mediated electrical responses in cultured cortical neurons isolated from rat. This finding suggests that TOPA quinone may play a role in pathological processes involving abnormal iron metabolism in catecholaminergic neurons.
2,4,5-三羟基苯丙氨酸（TOPA）在溶液中氧化形成一种醌衍生物，它是一种非NMDA谷氨酸能激动剂和神经毒素。多巴在生理溶液中可自动氧化形成少量的TOPA和TOPA醌。我们在此报告，这种转化可仅由铁（II）显著增强，但在过氧化氢存在下铁（II）的增强作用更明显。这种转化程度足以使生成的产物在从大鼠分离的培养皮层神经元中引发非NMDA、谷氨酸受体介导的电反应。这一发现表明，TOPA醌可能在涉及儿茶酚胺能神经元铁代谢异常的病理过程中起作用。
