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The decreased neuronal cell potential would lead to opening of voltage-gated Ca 2+ channels that would allow Ca 2+ , at 1.5 × 10 4 greater concentration outside the neuron compared to intraneuronal Ca 2+ concentration, to rush into the neuron, overwhelming intracellular storage sites and activating necrotic and apoptotic pathways (6, 139)

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Since previous studies have linked the activation of NRF2 with the repression of lipogenic gene expression 64 , we reasoned that GSH depletion causes oxidation and consequent inactivation of KEAP1 (a repressor of NRF2), thus leading to increased antioxidant and decreased lipogenic gene expression