The state of lipid peroxidation (LPO), respiration and oxidative phosphorylation, mitochondrial permeability transition pore (mPTP) and antiradical activity of rat liver mitochondria in streptozotocin (STZ)-induced diabetes condition were studied, considered the ways of correction of detected membrane damages with the use of gossitan, isolated from cotton plant Gossypium hirsutum L. It was shown that the rate of respiration of liver mitochondria in states V3 and V4 increases during STZ-induced diabetes, which significantly reduces the respiratory control (RC) and ADP/O coefficients in comparison with the control. The findings suggest that the uncoupling of respiration and oxidative phosphorylation takes place during STZ-induced diabetes. It was shown that in the conditions of STZ-induced diabetes, the rate of swelling of rat liver mitochondria is higher than of the healthy ones; this means that mPTP of rat liver mitochondria is in the open state. Gossitan recovers mPTP to the normal condition, thereby removing the effect of STZ on mitochondria. Gossitan (per os dose is 10 mg/kg of body weight, during 8 days) eliminates the detected functional disorders of rat liver mitochondria, probably due to its antioxidant properties.

In the current research paper, the flavonoid dihydroquercetin, 1-(2´-bromine-4´,5´-dimethoxyphenyl)-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline (F-18) and 2-(3,4-dihydroxyphenyl)-6-(1-(2´-bromine-4´, 5´-dimethoxyphenyl)-6,7-dimethoxy-3,4-dihydroisoquinoline-2 (1N)-il) methyl-3. The effects of 5,7-trigidroxychroman-4-on (DHQ-11) conjugate on rat liver mitochondrial calcium megachannels and on lipid peroxidation (LPO) induced using Fe2+/citrate were investigated in vitro experiments. White male rats weighing 180-200 grams were used in the experiments. It was found that the DHQ-11 conjugate was identified to have an inhibitory effect on rat liver mitochondria to calcium megachannels and peroxidation of lipids induced by Fe2+/citrate. The inhibitory properties of DHQ-11 conjugate on hepatic mitochondrial calcium megachannels and mitochondrial membrane lipid peroxidation were identified as active against dihydroquercetin and the F-18 isoquinoline alkaloid.