EFFECTS OF QUERCETIN AND DIHYDROQUERCETIN FLAVONOIDS ON CARDIAC MITOCHONDRIAL DYSFUNCTION

Abstract

Reduced cardiac mitochondrial respiration, disrupted membrane potential, and oxidative injury form an interconnected system, yet the effects of quercetin and dihydroquercetin on these processes remain inconsistently interpreted. The study aimed to compare the mechanistic influence of both flavonoids on the functional state, oxidative status, and membrane-related characteristics of isolated cardiac mitochondria. An experimental animal study used a factorial design, while liquid chromatography–mass spectrometry and high-performance liquid chromatography were applied to characterize the flavonoid composition. Mitochondrial respiratory activity, membrane potential, and oxidative-injury endpoints were assessed with standardized laboratory protocols. Between-group comparisons were performed using one-way and two-way analysis of variance followed by post-hoc testing. The resulting profile showed that quercetin and dihydroquercetin produced distinct changes in oxidative processes within cardiac mitochondria, but neither compound fully restored mitochondrial function under the examined conditions. Joint evaluation of respiration, membrane potential, and oxidative endpoints demonstrated that a single biomarker cannot adequately represent the mitochondrial response to flavonoid exposure. The scientific contribution lies in defining a multidimensional framework for comparing two flavonoids through coordinated chemical identification, functional measurement, and multifactor statistical analysis. This framework links compound identity with organelle-level responses without reducing mitochondrial dysfunction to one oxidative indicator. Future work should examine concentration–response relationships, chronic safety, and ischemia–reperfusion injury in intact myocardium. The findings establish a mechanistic basis for evaluating flavonoid-specific mitochondrial effects before therapeutic extrapolation.