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In this line, GSH depletion in glial cells, including astrocytes, leads to neuroinflammatory phenotype ( 2+ -dependent glutamate release from microglial cells is observed upon hypoxia-mediated redox imbalance likely via the activation of IP 3 R which could participate in excitotoxic damages during brain insults ( 2+ homeostasis and thus result in unregulated Ca 2+ -dependent release of factors as proinflammatory cytokines or glutamate endangering neuronal cell survival

Migdalska-Richards, A

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Taylor & Duodu, 2015)

2a) align well with the reduced -ketoglutarate concentrations disclosed by NMR analyses (Fig