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

A decrease in body temperature in homeothermic animals cancause a state of the body called hypothermic. It is accompaniedby the development of a number of pathological processes, many of whichare associated with mitochondrial dysfunction and the developmentof oxidative stress. In connection with the widespread introductionof hypothermia into medical practice, the question of the possibilityof a regulatory influence on the proxidant-antioxidant status ofmitochondria at low body temperatures remains relevant. In recentyears, plant polyphenols, in particular dihydroquercetin (DHQ),have gained wide popularity as therapeutic agents with antioxidantand membrane protective effects. In this work, we investigated theeffects of DHQ on the intensity of oxidative stress in rat liver mitochondriaunder moderate hypothermia. It was found that a course (5 days)oral administration of DHQ at a dose of 100 mg/kg significantlyreduces the levels of lipid peroxidation (LPO) and oxidative modificationof proteins (OMP) products in the liver mitochondria of controlrats, increasing the content of non-enzymatic components of thethiol-disulfide antioxidant system’s. DHQ effectively protects livermitochondria from the development of oxidative stress during hypothermia,as evidenced by a significant decrease (and in some cases, completenormalization) in the levels of diene conjugates, MDA, Schiff basesand carbonyl groups in a group of animals subjected to hypothermiawith prior administration of this polyphenol. At the same time,DHQ significantly increases the levels of glutathione and vitaminE, and also normalizes the content of thiol groups in mitochondrialproteins. In vitro, DHQ exhibits a dose-dependent antioxidant effect,suppressing OMB in mitochondria incubated in Fenton’s medium (IC₅₀ =0.160 mg/mL).