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Tissues with high metabolic activity would be predicted to produce higher levels of mitochondrial superoxide as a by-product of oxidative phosphorylation (Wallace, 2005) and be particularly subject to age-related disease

Eur J Clin Nutr 2000a;54(6):514-21

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Antioxidant therapy inhibits the TRPV1 channel by overexpressing GSH and GSHPx, while downregulating GSH and GSHPx promotes the TRPV1 channel [50,51,52]