Key result
In rats with doxorubicin-induced cardiomyopathy, the EPM-Mg complex significantly reduced heart tissue TBA-active products to 20.01 nmol/g compared to 37.42 nmol/g with doxorubicin alone.
Why the study?
The study was conducted to determine the effects of Tiotriasolin, Qudesan, and ubiquinone synthesis precursors on free radical processes and Krebs cycle dehydrogenases in rat heart and liver tissues during doxorubicin-induced cardiomyopathy.
Do metabolic compounds (Tiotriasolin, Qudesan, EPM-Mg) improve prooxidative-antioxidative balance and Krebs cycle enzyme activity in a rat model of doxorubicin-induced cardiomyopathy?
Do metabolic compounds (Tiotriasolin, Qudesan, EPM-Mg) improve prooxidative-antioxidative balance and Krebs cycle enzyme activity in a rat model of doxorubicin-induced cardiomyopathy?
Absolute Event Rate: 20.01% vs 37.42%
p-value: p=≤0.05
Metabolic compounds like ubiquinone-10 and its precursors may mitigate doxorubicin-induced cardiotoxicity by restoring oxidative balance and normalizing cellular energy metabolism in a preclinical model.
Reduces oxidative markers in doxorubicin rat hearts; leaves open any role in preventing clinical cardiotoxicity.
A study was conducted to determinate the effects of Tiotriasolin, Qudesan and the precursors of ubiquinone synthesis (EPM-Mg: alpha-tocopherol acetate), 4-hydroxybenzoic acid, methionine, Mg2+ ions) on the free radical processes and activity of some Krebs cycle dehydrogenases in rat heart and liver tissues under conditions of doxorubicin-induced cardiomyopathy. Administration of doxorubicin intensified the processes of lipid and protein oxidation and suppressed antioxidant enzymes activity in liver and heart tissues. Administration of metabolic correctional drugs caused a decrease the negative effect of doxorubicin on antioxidant system of heart and liver tissues due to increased activity of catalase and superoxide dismutase and inhibition of free radical processes. Doxorubicin administration caused an increase activity of both dehydrogenases in cardiomyocytes, which can be explained by triggering compensatory mechanisms in organ’s cells. The intake of metabolic drugs decreases the negative effect of anthracycline and approximates the dehydrogenase activity, which is close to the control values. In contrast to heart tissues, doxorubicin administration did not cause significant changes in the activity of energy enzymes in liver tissues, which may be due to the presence in the cells of liver a relatively powerful antioxidant defense system (capable in this experimental conditions effectively counteract doxorubicin-induced free radical processes). Administration of Qudesan and EPM-Mg caused a significant increase of alpha-ketoglutarate dehydrogenase and succinate dehydrogenase activities, which indicates the positive effect of these substances on work of the cell energy system.
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Dzuba et al. (2018) studied Doxorubicin-induced cardiomyopathy (n=30). Physiologically active compounds (Tiotriazoline, Qudesan, EPM-Mg) vs. Doxorubicin alone was evaluated on TBA-active products (TBARS) in heart tissue (nmol/g protein) (p=≤0.05). In rats with doxorubicin-induced cardiomyopathy, the EPM-Mg complex significantly reduced heart tissue TBA-active products to 20.01 nmol/g compared to 37.42 nmol/g with doxorubicin alone.
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