Shanker G, Aschner M
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1083, USA.
J Neurosci Res. 2001 Dec 1;66(5):998-1002. doi: 10.1002/jnr.10066.
Maintenance of appropriate intracellular glutathione (GSH) levels is crucial for cellular defense against oxidative damage. A suggested mechanism of methylmercury (MeHg) neurotoxicity implicates the involvement of oxygen radical formation and a decrease in cellular levels of GSH. Astrocytes play an important role in providing GSH precursors to neurons, and as will be discussed in this review, altered GSH homeostasis likely leads to impairment of astrocytic handling of glutamate, and neuronal energy metabolism. The review summarizes recent observations on transport systems for cysteine and cystine, precursors of GSH, in primary cultures of astrocytes and neurons, and their sensitivity to MeHg treatment.
维持适当的细胞内谷胱甘肽（GSH）水平对于细胞抵御氧化损伤至关重要。甲基汞（MeHg）神经毒性的一种推测机制涉及氧自由基的形成以及细胞内GSH水平的降低。星形胶质细胞在为神经元提供GSH前体方面发挥着重要作用，正如本综述中将讨论的那样，GSH稳态的改变可能导致星形胶质细胞对谷氨酸的处理以及神经元能量代谢受损。本综述总结了关于星形胶质细胞和神经元原代培养物中GSH前体半胱氨酸和胱氨酸转运系统的最新观察结果，以及它们对MeHg处理的敏感性。
