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Uptake of Glutamate and Cystine in C‐6 Glioma Cells and in Cultured Astrocytes
Author(s) -
Cho Yukie,
Bannai Shiro
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb05800.x
Subject(s) - glutamate receptor , cystine , glutathione , astrocyte , biochemistry , biology , glioma , chemistry , biophysics , microbiology and biotechnology , central nervous system , cysteine , endocrinology , enzyme , cancer research , receptor
The uptake of glutamate in rat glioma C‐6 cells and cultured astrocytes derived from rat cerebral hemispheres was found to be mediated by a Na + ‐dependent and a Na + ‐independent system. The Na + ‐dependent system was inhibited by aspartate and was consistent with the commonly occurring system designated system X − ag . The Na + ‐independent system was inhibited by cystine and was consistent with system x − c described in various types of cells in the periphery. It was also found that quisqualate selectively and competitively interfered with the Na + ‐independent glutamate uptake. In C‐6 cells, the glutamate uptake via systems X − ag and x − c accounted for approximately 35% and 55% of the total uptake, respectively, at 0.05 m M glutamate. In cultured astrocytes, the glutamate uptake via system X − ag was very potent, whereas the uptake via system x − c was relatively weak and its contribution to the total uptake of glutamate seemed almost negligible. However, in both C‐6 cells and astrocytes, system x − c was necessary for the uptake of cystine, another substrate of system x − c . Cystine in the culture medium was an essential precursor of glutathione, and the inhibition of the cystine uptake by excess glutamate as a competitor led to a severe deficiency in glutathione, followed by cell degeneration.