We are analyzing https://link.springer.com/article/10.1007/s11064-006-9077-z.

Title:
Ascorbate Transport and Recycling by SH-SY5Y Neuroblastoma Cells: Response to Glutamate Toxicity | Neurochemical Research
Description:
Neurons maintain relatively high intracellular concentrations of vitamin C, or ascorbic acid. In this work we studied the mechanisms by which neuronal cells in culture transport and maintain ascorbate, as well as how this system responds to oxidant stress induced by glutamate. Cultured SH-SY5Y neuroblastoma cells took up ascorbate, achieving steady-state intracellular concentrations of 6 mM and higher at extracellular concentrations of 200 μM and greater. This gradient was generated by relatively high affinity sodium-dependent ascorbate transport (K m of 113 μM). Ascorbate was also recycled from dehydroascorbate, the reduction of which was dependent on GSH, but not on d-glucose. Glutamate in concentrations up to 2 mM caused an acute concentration-dependent efflux of ascorbate from the cells, which was prevented by the anion channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. Intracellular ascorbate did not affect radiolabeled glutamate uptake, showing absence of heteroexchange.
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Topics {✒️}

kendra hayslett & zhi-chao qu 6-bromo-6-deoxy-l-ascorbic acid sh-sy5y neuroblastoma cells high-affinity sodium-dependent mechanism month download article/chapter oxidant stress induced glutamate-induced oxidative stress human neuron-astrocyte 3d transforming growth factor-β inhibits hypoxia-induced damage ischemia-induced neuronal damage acute concentration-dependent efflux glutamate-induced neuronal death ascorbic-acid transporter slc23a1 nitrosourea anti-tumor drugs astrocyte glutamate transport rat blood–retinal barrier human neuroblastoma cells active site-specific inhibition full article pdf modulating oxidative stress vanderbilt diabetes research dopamine d2l receptors glutathione-dependent reduction privacy choices/manage cookies wilson jx ascorbate transport activity ascorbic acid transport central nervous system ascorbic acid uptake sodium-chloride component physiologically induced release dehydroascorbic acid uptake na+-dependent vitamin ascorbate induces expression free radical production free radical formation glutathione redox cycle high intracellular concentrations related subjects intracellular ascorbic acid hl-60 cells depleted ascorbate analog specific ascorbate inhibits edema dehydroascorbic acid measurements brain ascorbic acid human cerebrospinal fluid α-lipoic acid european economic area oxidative stress

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         description:Neurons maintain relatively high intracellular concentrations of vitamin C, or ascorbic acid. In this work we studied the mechanisms by which neuronal cells in culture transport and maintain ascorbate, as well as how this system responds to oxidant stress induced by glutamate. Cultured SH-SY5Y neuroblastoma cells took up ascorbate, achieving steady-state intracellular concentrations of 6 mM and higher at extracellular concentrations of 200 μM and greater. This gradient was generated by relatively high affinity sodium-dependent ascorbate transport (K m of 113 μM). Ascorbate was also recycled from dehydroascorbate, the reduction of which was dependent on GSH, but not on d-glucose. Glutamate in concentrations up to 2 mM caused an acute concentration-dependent efflux of ascorbate from the cells, which was prevented by the anion channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. Intracellular ascorbate did not affect radiolabeled glutamate uptake, showing absence of heteroexchange.
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      description:Neurons maintain relatively high intracellular concentrations of vitamin C, or ascorbic acid. In this work we studied the mechanisms by which neuronal cells in culture transport and maintain ascorbate, as well as how this system responds to oxidant stress induced by glutamate. Cultured SH-SY5Y neuroblastoma cells took up ascorbate, achieving steady-state intracellular concentrations of 6 mM and higher at extracellular concentrations of 200 μM and greater. This gradient was generated by relatively high affinity sodium-dependent ascorbate transport (K m of 113 μM). Ascorbate was also recycled from dehydroascorbate, the reduction of which was dependent on GSH, but not on d-glucose. Glutamate in concentrations up to 2 mM caused an acute concentration-dependent efflux of ascorbate from the cells, which was prevented by the anion channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. Intracellular ascorbate did not affect radiolabeled glutamate uptake, showing absence of heteroexchange.
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         Dehydroascorbate reduction
         Glutamate uptake
         Excitotoxicity
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         Neurochemistry
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