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By activating Sxc , a key component in the control of extracellular glutamate, and inducing GLT1, NAC prevents excessive and neurotoxic glutamate release from excitatory nerve endings

Alok, S., Jain, S

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In conclusion, we show that APAP toxicity in HepG2 cells is largely independent of oxidative stress, and is linked instead to a decoupling of glycolysis from the TCA cycle, lactic acidosis, reduced NADPH production, and subsequent suppression of the anabolic pathways required for rapid growth