| Abstrakt: |
Abstract—In this work, we compared the efficacy of quercetin, one of the best known and widely investigated flavonoids, and the inclusion complex of quercetin and hydroxypropyl−β-cyclodextrin in prevention of disturbances in redox balance of rat liver mitochondria and erythrocytes during oxidative stress and regulation of the process of the mitochondrial permeability transition pore formations in vitro and theoretically calculated the structure of quercetin and its oxidative forms, as well as their molecular electronic properties. Quercetin (5-100 μM) inhibited membrane lipid peroxidation and reduced glutathione oxidation dose dependently in both rat liver mitochondria and erythrocytes during exposure to tert-butyl hydroperoxide (700 μM). Simultaneously, quercetin (25 μM) stimulated the Ca2+-induced mitochondrial permeability transition pore formations and inhibited this process at higher concentrations (100 mM). The incorporation of quercetin in the supramolecular complex with hydroxypropyl−β-cyclodextrin enhanced its antioxidative activity, first of all, in the cytoplasm of the cell and mitochondrial matrix. Molecules of quercetin, semiquinone radicals, and stable products formed in the oxidation, ortho- and p-quinone methide, have a planar structure. The calculated value of the dipole moment of the quercetin molecule is 4.34 D. The quercetin molecule is thermodynamically more stable than the products of its oxidation, among which p-quinone methide-III is the most stable form. [ABSTRACT FROM AUTHOR] |
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