Identification and characterization of uptake systems for cystine and cysteine in cultured astrocytes and neurons: Evidence for methylmercury-targeted disruption of astrocyte transport
Article first published online: 30 NOV 2001
Copyright © 2001 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 66, Issue 5, pages 998–1002, 1 December 2001
How to Cite
Shanker, G. and Aschner, M. (2001), Identification and characterization of uptake systems for cystine and cysteine in cultured astrocytes and neurons: Evidence for methylmercury-targeted disruption of astrocyte transport. J. Neurosci. Res., 66: 998–1002. doi: 10.1002/jnr.10066
- Issue published online: 30 NOV 2001
- Article first published online: 30 NOV 2001
- Manuscript Accepted: 22 AUG 2001
- Manuscript Revised: 3 AUG 2001
- Manuscript Received: 19 MAY 2001
- USPHS-NIH. Grant Number: NIEHS 07331
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. © 2001 Wiley-Liss, Inc.