The state of the mitochondrial megapore (mitochondrial permeability transition pore-mPTP), respiration and oxidative phosphorylation of rat liver and pancreas mitochondria in streptozotocin (STZ) -induced diabetes were studied, considered the ways of correction of the detected membrane damage with the flavone luteolin isolated from the plant Inula caspica. It was shown that, under conditions of experimental diabetes mellitus, the rate of swelling of rat liver and pancreas mitochondria is higher than of the healthy ones; this means that mPTP of rat liver and pancreas mitochondria is in the open state in pathology. Luteolin recovers mPTP to the normal condition, thus removing the effect of STZ on mitochondria. It was also shown that, the respiration rate of liver and pancreatic mitochondria in the state 3 and state 4 states increases in STZinduced diabetes, which significantly reduces the respiratory control (RC) and ADP/O coefficients in comparison with the control. The data obtained indicate the disconnection of respiration and oxidative phosphorylation in STZ -induced diabetes. Luteolin (oral dose is 50 mg/kg of body weight, during 8 days) eliminates the detected functional disorders of rat liver and pancreas mitochondria, probably due to its antioxidant properties.

In this study, the effects of 1,2,3-triazo derivatives on the amount of lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD), catalase activity in rat liver homogenate under the conditions of alloxan diabetes were studied.New derivatives of triazoles, TF-25, TS-27 and TB-31, were found to inhibit MDA content in rat liver homogenate and increase activity of antioxidant enzymes SOD and catalase in alloxan diabetes.

In this study, in vitro and in vivo experiments, it was studied soforaflavonozide (SFL) isolated from Alhagi canescens (Regel) B. Keller & Shap (Fabaceae (Leguminosae)), and narcissine isolated from Crocus sativus L. belonging to Iridaceae family. It was studied the effect of narcissine isolated from the plant on ATP-dependent potassium channel (mitoK ATP -channel) activity in rat cardiac mitochondria. Animals of experimental group were divided into 4 groups: I control group (healthy), II experimental group (ischemia model), III experiment group (ischemia + narcissin), IV experimental group (ischemia + SFL). In rats with ischemia a 0.1 ml 0.1% solution of 100 mg/kg adrenaline was administered subcutaneously and peritoneally for 3 days in relative to body weight. The rats that underwent the ischemia model were given oral administration of 10 mg/kg of narcissine flavonoid to group III and 10 mg/kg of SFL flavonoid to group IV orally for 7 days. After that, in the experimental animals carried out electrocardiogram. Mitochondria from rat heart tissue were isolated by differential centrifugation. Cardiac mitoK ATP -channel activity in the presence of ATP in an incubation medium was studied at concentrations of 10-50 µM of SFL and narcissine. Concentrations of 50 µM of SFL and narcissus and 30 µM of diazoxide were also found to have an activating effect on the mitochondrial channel of the heart. In the adrenaline-induced ischemia model, it was found that narcissine and SFL flavonoids restored the mitochondrial conduction permeability of the rat heart.

In current scientific article, rat liver mitochondria respond to the flavonoids dihydroquercetin (20-100 µM), 1-(2´bromo-4´,5´-dimethoxyphenyl)-6,7-dimethoxy-1,2,3,4 for respiratory and processes of oxidative phosphorylationtetrahydroisoquinolines F-18 (20-100 μM) and synthesized on the basis of followings 2-(3,4-dihydroxyphenyl)-6-[1-(2'-bromo-4',5'-dimethoxyphenyl)-6,7-The effect of dimethoxy-3,4-dihydroisoquinolin-2(1H)-yl]methyl-3,5,7-trihydroxychroman-4-on the concentrations of the DHQ-11 conjugate (20-100 μM) was investigated in in vitro experiments. Experiments were conducted within 180-200 gram infertile white male rats. Mitochondrias from rat liver were isolated by the way of differential centrifugation. Concentrations of dihydroquercetin flavonoid 20, 60, 100 μM in FAD-dependent succinate oxidation in rat liver mitochondria were identified to be reliable respiratory control parameters and partially increased ADF/O value, the respiratory control coefficient as Chans demonstrated an increase in respiratory rate under the influence of the alkaloid F-18 isoquinoline 20, 60, 100 μM. Moreover, the ADP/O coefficients also boosted under the influence of the isoquinoline alkaloid F-18. It was observed that ADP/O ratio coefficients was expanded within the bonding by the effect of the DHQ-11 conjugate concentration. The concentration of 100 μM dihydroquercetin for FAD-dependent succinate oxidation in rat liver mitochondria surged Chance's respiratory rate by 15% compared to the control. Concentrations of isoquinoline alkaloid F-18 100 μM enlarged the respiratory rate by 13% compared to the control. It was defined that concentrations of 100 μM DHQ-11 conjugate rose the respiratory rate by 20%. The oxidation of FAD-dependent substrates in mitochondria was more actively effected by the DHQ-11 conjugate than dihydroquercetin and F-18 isoquinoline alkaloids.