Biochemical properties of ubiquinone function under experimental pathological conditions of cardiovascular system

The aim of this project was to study the state of mitochondrial electron-transport chain components, CoQ content and sensitivity of mitochondrial permeability transision pore in rat heart mitochondria under treatment with adrenaline, doxorubicin, and complexes of modulators and precursors of CoQ biosynthesis. Subsequent application of complexes of precursors and modulators of ubiquinone biosynthesis under the adrenaline treatment decreases in sensitivity of mitochondrial permeability transition pore to inductors of its opening, improves activities of the mitochondrial electron-transport chain complexes I, II and IV. These complexes can act as effective anti-hypoxic remedies that promote normalization of the energy metabolism in heart. In the series of studies on rats treated with doxorubicin the administration of complexes of precursors and modulators of ubiquinone biosynthesis leads to significant decrease sensitivity of mitochondrial permeability transition pore to inductors of its opening and normalization of mitochondrial electron-transport chain function, which may lead to notable reduction of doxorubicin toxicity. The expiremental data obtained may become the basis of development of approaches to correction of adverse effects of doxorubicin by treatment with the complexes of precursors and modulators of its biosynthesis. These data may be used to substantiate the application of these biologically active substances within frameworks of complex treatment of cardiovascular pathologies.