The role of calcium-dependent processes in cardiac physiology and pathophysiology as well as the function of mitochondria as a regulator of myocyte calcium homeostasis have been extensively discussed. The aim of the present work was to evaluate the mechanism(s) of modulation of respiratory activity, morphology, permeability transition, and membrane potential of rat cardiac mitochondria by exogenous Ca2+ ions in the absence or in the presence of the plant flavonoid glucoside naringin. Low free Ca2+ concentrations (40–250 nM) effectively inhibited the respiratory activity of rat heart mitochondria: decreased the rates of succinate-dependent V2 and ADP-stimulated V3 respiration, remaining unaffected the efficacy of oxygen consumption. In the presence of high exogenous Ca2+ ion concentrations (the free Ca2+ concentration was 550 µM), we observed a dramatic increase in mitochondrial heterogeneity in size and electron density that was connected with calcium-induced opening of the mitochondrial permeability transition pores (MPTP) and membrane depolarization, observed at free Ca2+ concentrations of 150 to 750 µM. As compared to rat liver mitochondria, the sensitivity to Ca2+ of rat heart mitochondria was much lower in the case of MPTP opening and much higher in the case of respiration inhibition. Naringin, occurring naturally in citrus fruits, partially prevented Ca2+-induced rat cardiac mitochondrial morphological transformations (200 µM), dose-dependently inhibited the respiratory activity of mitochondria (10–75 µM) in the absence or in the presence of calcium ions and promoted membrane potential dissipation and mitochondria swelling in the absence of calcium ions but inhibited calcium-induced MPTP formation at higher concentrations (75 µM).

Aim The liver is the main target for alcohol-induced injury. The aims of this work were to carry out further research into the mechanisms of liver damage induced by long-term administration of high-dose ethanol to rats and to evaluate the hepatoprotective potential of red cabbage (Brassica oleracea var. capitata f. rubra) anthocyanins (RCE). Material/Methods Male albino Wistar rats were divided into four groups. Group 1 was the control. Groups 2 through 4 received ethanol (4 g/kg body weight, 8 weeks). Group 3 received 11 mg RCE/kg and Group 4 received 22 mg RCE/kg. Dry lyophilised RCE was prepared from fresh red cabbage and analysed. We then evaluated the liver histology, mitochondrial respiration, and biochemical and immunological parameters in these groups of rats. Results The rat intoxication caused steatohepatitis characterised by macro- and microvesicular steatosis, ballooning and fatty liver dystrophies, lymphocytic infiltration, neutral lipid accumulation, and elevations of the serum activities of the liver injury marker enzymes. The treatment of alcohol-administered rats with RCE (mainly, cyanidin-3-diglucoside-5-glucoside, cyanidin-3-coumaroylrutinoside-5-hexoside, cyanidin-3-feruloylrutinoside-5-hexoside, delphinidin-3-feruloylrutinoside-hexoside) dose-dependently alleviated these pathological changes: The sizes of hepatocyte lipid vacuoles and the inflammatory signs were decreased, and the levels of the rat serum biochemical markers of liver injury, proinflammatory cytokines TNFα and IL-6, and the adipokine leptin (and not TGFβ) were significantly reversed. The RCE administration during intoxication completely recovered the changed liver mitochondria respiration rates and the ADP/O coefficient, as well as the phagocytic index and neutrophil metabolic activity in the blood. In experiments in vitro, RCE (13.6 μg/ml) modulated the respiratory parameters of isolated rat liver mitochondria, dissipated mitochondrial membrane potential, and inhibited the Ca2+-induced mitochondrial permeability transition. Conclusion The red cabbage anthocyanins could be useful for treatment of alcoholic liver injury due to their Ca2+-ionophoric/protonophoric activity, influence on Ca2+ homeostasis, and improving mitochondrial functions and inflammatory status.