Abstract

One of the widespread public health problems nowadays is toxic liver damage. The key mechanism of the pathogenic action of xenobiotics One of the widespread public health problems nowadays is toxic liver damage. The key mechanism of the pathogenic action of xenobiotics on the liver is the activation of oxidative stress. Excessively generated free radicals damage mitochondrial components in hepatocytes, which can lead to disfunc-tion of mitochondrial dehydrogenases. The aim of the work was to investigate the influence of antioxidant 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline on oxidative status, activity of succinate dehydrogenase and NAD-dependent malate dehydrogenase in rats with toxic liver damage. Material and methods. The study included 48 male Wistar rats weighing 200-250 g, divided into 4 groups of 12 animals in each: control group, a group of animals with tetrachloromethane-induced liver damage, rats with pathology that received intragastrically 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline at a dose of 50 mg/kg, and control rats received the tested compound. The level of oxidative modification of proteins was assessed by the method of Reznick et al. with slight modifications, alpha-tocopherol concentration was estimated by the method based on measuring the ab-sorption of chromogenic complex compound Fe2+ and orthophenanthroline. Activity of alanine aminotransferase, aspartate aminotransferase and gamma-glutamyltranspeptidase was determined in blood serum using Olvex Diagnosticum reagent kits (Russia, Saint Petersburg). Cytoplasmic and mitochondrial liver fractions were obtained for analysis of succinate dehydrogenase and NAD-dependent malate dehydrogenase activity. Results. Results of the work have shown that 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline treatment led to the normalization of the analyzed pa-rameters, which was apparently due to the correction of the redox status in the liver of animals under the action of the tested compound. Conclusion. The results of the study make it necessary to further investigate the effect of dihydroquinoline derivatives on oxidative metabolic en-zymes in pathological

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