An endogenous metal appears to regulate NMDA receptor mediated 45Ca influx and toxicity in cultured cerebellar granule cells
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γ-Glutamylcysteine ameliorates oxidative injury in neurons and astrocytes in vitro and increases brain glutathione in vivo
2011, NeuroToxicologyCitation Excerpt :Although the main effects of NAC are thought to arise from its deacetylation into cysteine, the rate-limiting substrate for GSH synthesis (Lauterburg et al., 1983), both of these GSH precursors have potential neurotoxic side effects (Puka-Sundvall et al., 1995). Indeed, both NAC and cysteine potentiate glutamate toxicity in cultured cerebellar granule cells (Eimerl and Schramm, 1992). Similarly, cysteine elevates the influx of Ca2+ in cultured granule cells and causes neurotoxicity in the neonatal rat brain under in vivo conditions (Janáky et al., 1993; Lehmann et al., 1993).
Brain injury after neonatal hypoxia-ischemia in rats: A role of cysteine?
1998, Brain ResearchBicarbonate-sensitive cysteine induced elevation of extracellular aspartate and glutamate in rat hippocampus in vitro
1997, Neurochemistry InternationalCa<sup>2+</sup> influx through glutamate receptor-associated channels in retina cells correlates with neuronal cell death
1996, European Journal of PharmacologyNeurotoxicity of cysteine: interaction with glutamate
1995, Brain Research
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