Effects of Dihydroquercetin on the Intensity of Oxydative Stress in Rat Liver Mitochondria at Hypothermia

A decrease in body temperature in homeothermic animals can cause a state of the body called hypothermic. It is accompanied by the development of a number of pathological processes, many of which are associated with mitochondrial dysfunction and the development of oxidative stress. In connection with the widespread introduction of hypothermia into medical practice, the question of the possibility of a regulatory influence on the proxidant-antioxidant status of mitochondria at low body temperatures remains relevant. In recent years, plant polyphenols, in particular dihydroquercetin (DHQ), have gained wide popularity as therapeutic agents with antioxidant and membrane protective effects. In this work, we investigated the effects of DHQ on the intensity of oxidative stress in rat liver mitochondria under moderate hypothermia. It was found that a course (5 days) oral administration of DHQ at a dose of 100 mg/kg significantly reduces the levels of lipid peroxidation (LPO) and oxidative modification of proteins (OMP) products in the liver mitochondria of control rats, increasing the content of non-enzymatic components of the thiol-disulfide antioxidant system’s. DHQ effectively protects liver mitochondria from the development of oxidative stress during hypothermia, as evidenced by a significant decrease (and in some cases, complete normalization) in the levels of diene conjugates, MDA, Schiff bases and carbonyl groups in a group of animals subjected to hypothermia with prior administration of this polyphenol. At the same time, DHQ significantly increases the levels of glutathione and vitamin E, and also normalizes the content of thiol groups in mitochondrial proteins. In vitro, DHQ exhibits a dose-dependent antioxidant effect, suppressing OMB in mitochondria incubated in Fenton’s medium (IC 50 = 0.160 mg/mL).