The multifaceted role of quercetin derived from its mitochondrial mechanism.

Abstract

Quercetin is a flavonoid with promising therapeutic applications; nonetheless, the phenotype exerted in some diseases is contradictory. For instance, anticancer properties may be explained by a cytotoxic mechanism, whereas antioxidant-related neuroprotection is a pro-survival process. According to the available literature, quercetin exerts a redox interaction with the electron transport chain (ETC) in the mitochondrion, affecting its membrane potential. It also affects ATP generation by oxidative phosphorylation, where ATP deprivation could partly explain its cytotoxic effect. Moreover, quercetin may support the generation of free radicals through redox reactions, causing a prooxidant effect. The nutrimental stress and prooxidant effect induced by quercetin might promote pro-survival properties such as antioxidant processes. Thus, in this review, we discuss the evidence supporting that quercetin redox interaction with the ETC could explain its beneficial and toxic properties.