ubiquinone and kaempferol

Ubiquinone (coenzyme Q) is a vital respiratory cofactor and liposoluble antioxidant. Studies have shown that plants derive approximately a quarter of 4-hydroxybenzoate, which serves as the direct ring precursor of ubiquinone, from the catabolism of kaempferol. Biochemical and genetic evidence suggests that the release of 4-hydroxybenzoate from kaempferol is catalyzed by heme-dependent peroxidases and that 3-O-glycosylations of kaempferol act as a negative regulator of this process. These findings not only represent an atypical instance of primary metabolite being derived from specialized metabolism but also raise the question as to whether ubiquinone contributes to the ROS scavenging and signaling functions already established for flavonols.

Topics: Kaempferols; Plants; Ubiquinone

Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and an important antioxidant present in all cellular membranes. CoQ deficiencies are frequent in aging and in age-related diseases, and current treatments are limited to CoQ supplementation. Strategies that rely on CoQ supplementation suffer from poor uptake and trafficking of this very hydrophobic molecule. In a previous study, the dietary flavonol kaempferol was reported to serve as a CoQ ring precursor and to increase the CoQ content in kidney cells, but neither the part of the molecule entering CoQ biosynthesis nor the mechanism were described. In this study, kaempferol labeled specifically in the B-ring was isolated from

Topics: Animals; Antioxidants; Ataxia; Epithelial Cells; Flavonols; Humans; Kaempferols; Kidney; Mice; Mitochondria; Mitochondrial Diseases; Mitochondrial Membranes; Muscle Weakness; Mutation; Ubiquinone

Land plants possess the unique capacity to derive the benzenoid moiety of the vital respiratory cofactor, ubiquinone (coenzyme Q), from phenylpropanoid metabolism via β-oxidation of

Topics: Arabidopsis; Gene Expression Regulation, Plant; Kaempferols; Parabens; Plants; Solanum lycopersicum; Ubiquinone

Coenzyme Q (Q) is a lipid-soluble antioxidant essential in cellular physiology. Patients with Q deficiencies, with few exceptions, seldom respond to treatment. Current therapies rely on dietary supplementation with Q

Topics: Animals; Antioxidants; Carbon Isotopes; Cell Line; Epithelial Cells; Fibroblasts; HEK293 Cells; Hep G2 Cells; HL-60 Cells; Humans; Isotope Labeling; Kaempferols; Kidney Tubules, Proximal; Mice; Mitochondria; Polyphenols; Saccharomyces cerevisiae; Sirtuin 3; Ubiquinone

Flavonoids can protect cells from different insults that lead to mitochondria-mediated cell death, and epidemiological data show that some of these compounds attenuate the progression of diseases associated with oxidative stress and mitochondrial dysfunction. In this work, a screening of 5 flavonoids representing major subclasses showed that they display different effects on H₂O₂ production by mitochondria isolated from rat brain and heart. Quercetin, kaempferol and epicatechin are potent inhibitors of H₂O₂ production by mitochondria from both tissues (IC₅₀ approximately 1-2 μM), even when H₂O₂ production rate was stimulated by the mitochondrial inhibitors rotenone and antimycin A. Although the rate of oxygen consumption was unaffected by concentrations up to 10 μM of these flavonoids, quercetin, kaempferol and apigenin inhibited complex I activity, while up to 100 μM epicatechin produced less than 20% inhibition. The extent of this inhibition was found to be dependent on the concentration of coenzyme Q in the medium, suggesting competition between the flavonoids and ubiquinone for close binding sites in the complex. In contrast, these flavonoids did not significantly inhibit the activity of complexes II and III, and did not affect the redox state of complex IV. However, we have found that epicatechin, quercetin and kaempferol are able to stoichiometrically reduce purified cytochrome c. Our results reveal that mitochondria are a plausible main target of flavonoids mediating, at least in part, their reported preventive actions against oxidative stress and mitochondrial dysfunction-associated pathologies.

Topics: Animals; Antimycin A; Antioxidants; Apigenin; Brain; Catechin; Cytochromes c; Electron Transport Complex I; Flavonoids; Heart; Hydrogen Peroxide; Kaempferols; Mitochondria; Oxidants; Oxidation-Reduction; Oxygen Consumption; Quercetin; Rats; Rats, Wistar; Rotenone; Ubiquinone; Uncoupling Agents