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Abstract

How could quercetin exert a pro-survival phenotype (antioxidant) in mammalian cells while toxic to other eukaryotic cells? The redox capacity of quercetin may explain its antioxidant and toxic effects, based on the idea that quercetin impairs the electron transport chain, affecting ATP production and forming quercetin-derived free radicals. Herein, we provide evidence that quercetin supplementation: 1) depolarizes the mitochondrial membrane and augments the ADP/ATP ratio; 2) increases superoxide anion cellular levels; 3) changes the cellular response to H2O2 challenge associated with the antioxidant cellular response; 4) sensitizes the cellular response to lipoperoxidation challenge, and 5) augments cardiolipin levels. These events suggest that the quercetin pro-oxidant effect is related to mitochondrial respiration dysfunction and could induce cellular antioxidant response.

Citations
4
FWCI
1.43
Field percentile
top 23%

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