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Functional analyses of vitamin C uptake in C17.2 neural precursor cells (SVCT2 +) show the existence of a saturable uptake mechanism for AA, which is sodium-dependent (Km 40 M) (Tsukaguchi et al., 1999

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These signals trigger the inflammasome, intensifying the inflammatory response and accelerating hepatocyte necrosis and apoptosis [4, 92, 93]

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