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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

Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells

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The timing of injection relative to meals and other activities may influence tolerance and efficacy