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Results Inhibition of glutathione metabolism depletes neuronal glutamate and affects excitatory transmission To test the hypothesis that glutathione is a significant reservoir for glutamate, we treated neuronal cells with molecular inhibitors targeting enzymes of the glutathione metabolic cycle: L-2-imidazolidone-4-carboxylate (2I4C), acivicin, L-buthionine sulfoximine (BSO), and sulforaphane

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Patients who see the best results treat GHK-Cu as a non-negotiable part of their daily evening routine, not as an optional treatment

In general, patients are hospitalized in an acute care facility for acetylcysteine therapy