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Cardiomyopathies are among the most severe myocardial pathologies, which are characterized by resistance to therapy and high mortality due to increasing heart failure and arrhythmia. Cardiomyocyte pathological changes upon cardiomyopathies are associated with mitochondrial dysfunction, leading to excessive formation of reactive oxygen species and the development of oxidative stress. In this regard, the study of the therapeutic potential of antioxidants in cardiomyopathies, as well as the mechanisms of their action on the functioning of mitochondria, is relevant and of high practical importance. The aim of this study was to determine the effect of oral 14-day administration of dihydroquercetin in a water-soluble form (DHQWF) on the activity of the key marker of mitochondrial respiration [succinate dehydrogenase (SDH)] and the cytoplasmic marker of glycolysis [lactate dehydrogenase (LDH)] in blood lymphocytes, as well as on the serum level of lipid peroxidation (LPO) in control rats and rats with experimental cardiomyopathy. Material and methods . Adult male Wistar rats (body weight 220-240 g) were used for the study. Isoprenaline hydrochloride was used to induce cardiomyopathy (IIC) in animals (twice subcutaneous injection at a dose of 150 mg/kg body weight, with a break of 24 hours). DHQ-WF was added to the drinking water for 14 days at the dose of 15 or 30 mg/kg body weight. SDH and LDH activity in lymphocytes was measured using a highly sensitive cytobiochemical method on a blood smear according to the reduction of nitrotetrazolium blue chloride to diformazan of dark blue color. The content of malone dialdehyde (MDA) in the blood serum, heart and liver mitochondria was determined spectrophotometrically using thiobarbituric acid. Mitochondria were isolated from rat tissues by the conventional method of differential centrifugation. Mitochondrial respiration was recorded using a polarographic method. Results . Experimental cardiomyopathy in rats was accompanied by a twofold increase in blood serum MDA level, as well as by a significant increase in SDH and LDH activity in blood lymphocytes. The oral administration of DHQ-WF in cardiomyopathy at a dose of 15 mg/kg body weight led to a significant decrease in serum MDA level, but did not reduce the activity of SDH and LDH in blood lymphocytes, compared with animals with cardiomyopathy that did not receive DHQ-WF. In the control group of animals, the use of DHQ-WF at a dose of 15 mg/kg body weight significantly increased blood lymphocyte LDH activity, but did not have a statistically significant effect on SDH activity and the parameters of mitochondrial respiration and oxidative phosphorylation, the level of MDA in heart and liver mitochondria. Increasing the dose of DHQ-WF administered to 30 mg/kg had less effect on changes in these parameters in control animals. Conclusion . The data obtained indicate that in experimental cardiomyopathy in rats, the course application of DHQ-WF at a dose of 15 mg/kg of body weight acts as an effective antioxidant that prevents the development of lipid peroxidation in blood serum, and can modulate energy metabolism towards the enhancement of glycolysis in blood lymphocytes in control animals., Competing Interests: The authors declare no overt and potential conflict of interest related to the publication of this article., (Copyright© GEOTAR-Media Publishing Group.)

Biological effects of light near infrared radiation (850 nm), with modulation acoustic frequency of 101 Hz, was studied. The study was conducted on rats, the effect was recorded by succinate dehydrogenase activity in lymphocytes on the blood smear after administration of the activating dose of adrenaline, which simulates the state of the organism in the early stages of the pathogenic effects (stress). A pronounced regulating effect of infrared radiation on the activity of succinate dehydrogenase in animals activated by adrenaline was shown. Infrared radiation has a normalizing effect reducing the degree of inhibition or activation of the enzyme induced by adrenaline and had no effect on the control animals. Thus, by modulating the activity of succinate dehydrogenase infrared radiation regulates energy production in the mitochondria supported by the most powerful oxidation substrate--succinic acid, which is especially pronounced under stress.