Search

Aim. To evaluate the functional state of mitochondria isolated from peripheral blood mononuclear leukocytes using flow cytometry in patients with chronic heart failure receiving ubidecarenone (coenzyme Q).Materials and methods. The study included 53 patients with chronic heart failure who had experienced myocardial infarction. The patients were divided into two groups: group 1 received optimally chosen standard therapy, while group 2 received optimally chosen standard therapy and ubidecarenone (“Kudevite”). The mitochondrial membrane potential was evaluated by flow cytometry using propidium iodide and 3,3′-dihexyloxacarbocyanine iodide (DiOC6(3)). The levels of coenzyme Q were determined using high-performance liquid chromatography with ultraviolet (UV) detection.Results. A direct correlation was established between the coenzyme Q levels in the blood plasma and the percentage of DiOC6(3)-positive cells (R = 0.39; р < 0.05) in the patients with chronic heart failure. In group 1, no significant differences in the coenzyme Q levels and the percentage of DiOC6(3)-positive and DiOC6(3)-negative cells before and after the therapy were observed. In group 2, a significant increase in the proportion of DiOC6(3)-positive cells and a significant decrease in the percentage of DiOC6(3)-negative cells were revealed.Conclusion. The increase in the functional activity of mitochondria in the patients with chronic heart failure receiving ubidecarenone was identified. Flow cytometry can be used to evaluate the functional state of mitochondria and observe the efficiency of the selected therapy.

Aim. To study the state of the antioxidant system in mitochondria of skin cells during B16/F10 melanoma growth in mice with chronic neurogenic pain.Materials and methods. The study included female С57ВL/6 mice (n = 28). Experimental groups included an intact group, a control group – chronic neurogenic pain model, a comparison group – standard subcutaneous transplantation of В16/F10 melanoma, and a main group – transplantation of В16/F10 melanoma 3 weeks after creation of a model of chronic neurogenic pain. Animals were decapitated on day 14 of the В16/F10 melanoma growth, the skin was excised and mitochondria were isolated. Standard ELISA test systems were used to determine the levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) (Bio Source, USA); glutathione peroxidase-4 (GPx 4) (Clod-Clon Corporation, CNDR); glutathione reductase (GR) (Cusabio, CNDR); glutathione S-transferase (G-S-T) (Ivvundiagnostik, Germany); glutathione peroxidase-1 (GPx 1), and superoxide dismutase-2 (SOD-2) (Ab Frontier, South Korea).Results. Mitochondria of skin cells in controls showed an increase in the levels of GSH by 1.3 times, GPx 1 – by 2.9 times, GPx 4 – by 1.9 times, GR – by 2.8 times, and SOD-2 – by 2.4 times, compared to intact animals. Changes in the comparison group were opposite: GPx 1 decreased by 1.9 times, GPx 4 – by 3.7 times, GR – by 3.9 times, SOD-2 – by 3.8 times, and GSSG rose by 1.36 times compared to intact animals. The growth of melanoma with chronic neurogenic pain caused an increase in the levels of GSH by 1.5 times, GPx 1 – by 3.6 times, G-S-T – by 1.28 times, GPx 4 – by 1.6 times, and SOD-2 – by 1.8 times, compared to intact animals.Conclusions. The growth of В16/F10 melanoma together with chronic neurogenic pain restructures the antioxidant system of skin mitochondria towards generation of reductive stress under the influence of chronic pain, which can affect the growth and development of experimental melanoma.

Autophagy is the main catabolic process required for the removal of damaged organelles, aggregated proteins and intracellular pathogens from cells. Oxidative stress is accompanied by an increase in autophagy, which has a protective effect by maintaining the qualitative composition of mitochondria (mitophagy) and peroxisomes (pexophagy) followed by lysosomal degradation of organelles with high production of reactive oxygen species. Aggrephagy also removes toxic products formed during oxidative and carbonyl stress. Furthermore, autophagy can activate the antioxidant response element system and increase the expression of antioxidant enzyme genes. The protective role of autophagy can be useful in many pathological processes accompanied by the development of oxidative stress while at the same time it may cause chemoresistance, reducing the effectiveness of anti-tumor therapy.

The rate of oxygen uptake by heart mitochondria (Mch) at different heart pathologies (myocardial infarction, diabetes mellitus and their combination) was studied polarographically. The rate of oxygen uptake of damaged heart Mch and content of free fatty acids (FFA) were increased. Change of these parameters was increased with the development of pathologies that is most pronounced in the groups «diabetes» and «diabetes + myocardial infarction». In the group of «myocardial infarction + diabetes» pathological process was developed less intensively in comparison with individual pathologies. Addition of FFA suppressed the rate of oxygen uptake of Mch. Equally, inhibition of phospholipase A2 suppressed the respiration of Mch. The hypothesis that FFA act as modulators of the activity of phospholipase A2 was discussed.

The influence of hepatoprotector phospholipid nature Essentiale and Essenciale combination with succinic acid on the metabolism of liver injury caused by Paracetamol in rats has been investigated. As a result of therapy was decreased Paracetamol hepatotoxicity — in the blood reduced the aminotransferases, alkaline phosphatase activity, bilirubin content, in liver homogenates decreased production of diene conjugates, Schiff bases and malondialdehyde. Essentiale improved the oxidative phosphorylation conjugacy without influence on liver mitochondria respiratory activity kinetic parameters. Combined application of Essentiale and succinic acid normalized the liver mitochondria respiratory function.