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These include (1) using GLUD1 for NAD(P)H generation during glutamate conversion to -ketoglutarate instead of GOT2 that does not generate NAD(P)H, (2) increasing NNT function by increasing the levels of its substrate NADH, which occurs during times of fasting or DR as a result of an increased rate of astrocyte fatty acid and beta-hydroxybutyrate oxidation and the reduced mitochondrial [NAD + ]/[NADH], (3) increasing the NADPH-generating flux from isocitrate through IDH2 instead of the NADH-generating flux through IDH3, or (4) increasing cataplerotic NAD(P)H-generating malic enzyme 2 (ME2) and NADPH-generating malic enzyme 3 (ME3) activities together with maintaining anaplerotic pyruvate carboxylase (PC) activity, which converts pyruvate to oxaloacetate, to balance the ME2 and ME3-mediated cataplerosis

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Both in vitro and in vivo studies have confirmed the protection of the alveolar epithelium from oxygen radical toxicity by treatment with NAC