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Understanding the transport of GSH across the plasma membrane is an important issue that is essential to treatment of diseases involving oxidative stress (see reviews by Ballatori et al., 2008 and by Yuan and Kaplowitz, 2008 in this issue)

Thus, we tested whether supplementation with the GSH precursor downstream of L-cysteine, -GCS, could affect cell viability following glucose deprivation

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Ischemic stroke-induced excessive zinc release from synaptic vesicles triggers excitotoxicity that moves into post-synaptic neurons through calcium-permeable channels, such as GluR and calcium-permeable AMPA/K (Ca-A/K)

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