Введение. Гипергомоцистеинемия-патогенетический фактор ряда заболеваний. Печень-ключевой орган в обмене гомоцистеина. Цель исследования-изучить структуру печени крыс при гипергомоцистеинемии. Материалы и методы. Гипергомоцистеинемию вызывали нагрузкой метионином. Печень подвергали морфологическому исследованию. Результаты. Гипергомоцистеинемия индуцирует локальные структурные изменения микроциркуляторного русла печени, стимулирует фиброгенез. Основной популяции гепатоцитов присущи морфологические признаки, указывающие на возрастание биосинтетического и энергетического потенциала клеток. В части гепатоцитов отмечаются дистрофические изменения, затрагивающие в основном ядерный аппарат и митохондрии. Регистрируются особенные структурные изменения митохондрий и эндоплазматического ретикулума гепатоцитов. Заключение. Выявлены специфические изменения структуры печени при гипергомоцистеинемии, вызванной нагрузкой метионином.

The effect of methionine overload on the state of the pool of sulfur-containing amino acids and their metabolites was studied in the various brain structures determined by reverse phase high performance liquid chromatography (HPLC). In all regions of the brain studied, methionine led to a unidirectional imbalance of sulfur-containing compounds: there was an increase in the concentrations of methionine, cystathionine and hypotaurine. The most pronounced increase in methionine and hypotaurine levels was observed in the striatum, cystathionine in the hemispheres. A significant increase in taurine concentration was observed only in the hypothalamus and striatum. In other parts of the brain a tendency to increase its level was shown. In all brain regions studied except the striatum, serine levels were decreased. In the cerebellum, in comparison with other regions, an increase in the level of cysteic acid and a decrease in the level of cysteinesulfinic acid were observed, which indicates that taurine synthesis is occurred mainly through the cysteine sulfinate oxidation.

Background. The content of retinol and α-tocopherol in the human body affects the development and progression of chronic liver diseases and is associated with the functioning of perisinusoidal lipocytes (HSC) and the state of biological membranes. Objective – to evaluate the content of retinol and α-tocopherol in blood plasma and liver tissue in the dynamics of experimental liver fbrosis in rats. Material and methods. Modeling of liver fbrosis / cirrhosis was carried out on sexually mature male rats by intraperitoneal administration of thioacetamide (TAA) solution at a dose of 200 mg / kg every other day for 4 and 12 weeks. The control group of animals received an equal volume of saline. The concentration of α-tocopherol and retinol was determined by S.L. Taylor’s method. Results. In rat liver preparations, 4 weeks after administration of TAA solution to animals, signs of FII-III stage of fbrosis were observed. According to electron microscopy, HSCs were in a transitional state and acquired a more elongated shape; the number of lipid inclusions in their cytoplasm decreased. The administration of TAA for 12 weeks led to the formation of liver cirrhosis in rats, with characteristic macro- and microscopic changes. On light microscopy, the number of HSCs decreased in rat liver preparations 3 months after administration of TAA; activated HSCs were encountered, which acquired an elongated shape and lost lipid inclusions. The content of retinol in the 2nd group of animals (with liver fbrosis stage II-III) was 2.2 times higher than in the control group, and 1.8 times higher than in the 3rd group with liver cirrhosis (p < 0.05). The content of retinol in the liver tissue after 4 weeks of TAA administration decreased by 11.7%, after 12 weeks - by 1.5 times. The level of α-tocopherol in the liver at the stage of fbrosis FII-III decreased by 21% compared with the control group, at the stage of cirrhosis - by 2 times. Conclusion. The use of thioacetamide in rats for 1 and 3 months leads to the development of liver fbrosis and cirrhosis. A decrease in the content of retinol and α-tocopherol in the liver occurs with the progression of liver fbrosis /cirrhosis. The high content of retinol and α-tocopherol in plasma at the stage of liver fbrosis FII-III is due to degranulation (activation) of HSC.

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