Abstract
Disruption of the metabolism of the essential amino acid methionine causes the syndrome of hyperhomocysteinemia. This pathological condition is associated with the risk of developing a number of diseases, including chronic liver disease. The mechanisms of liver tissue damage in hyperhomocysteinemia remain poorly understood and require more detailed study. The aim of the study is to establish the features of submicroscopic changes in the liver structure of old rats with hyperhomocysteinemia. The experimental study was performed on 22 white nonlinear old (24-26 months) male rats, which were divided into a control group and an experimental group. A model of persistent hyperhomocysteinemia was created by administering to rats of experimental group of thiolactone homocysteine at a dose of 200 mg/kg body weight intragastrically for 60 days. The study of ultrastructural changes in the lungs of rats was performed using an electron microscope PEM-125K. At experimental hyperhomocysteinemia in a liver of old rats there are changes in all structural components. Mitochondrial destruction and edema were observed in the vascular endothelium. Organelles have an enlightened matrix, a reduced number of cristae. A significant content of destructively altered mitochondria in endothelial cells indicates a failure of adaptation mechanisms. Erythrocyte sludges are observed in the lumens of the sinusoids. The number of fat-accumulating cells decreases, which indicates their transformation into fibroblasts and leads to the growth of collagen fibers, expansion of the sinusoidal spaces and the development of stromal fibrosis.
Highlights
The problem of chronic liver disease has become extremely relevant recently
It is known that homocysteine is a normal intermediate product of methionine metabolism, but under conditions of its excessive development, the syndrome of hyperhomocysteinemia (HHC) develops, which is associated with the risk of various pathological conditions
Destruction and edema of mitochondria are observed in the vascular endothelium
Summary
The problem of chronic liver disease has become extremely relevant recently. Due to its high growth and prevalence, scientists around the world note that chronic liver disease is the second epidemic of our century after the epidemic of cardiovascular disease. It is known that homocysteine is a normal intermediate product of methionine metabolism, but under conditions of its excessive development, the syndrome of hyperhomocysteinemia (HHC) develops, which is associated with the risk of various pathological conditions These include non-alcoholic fatty liver disease, coronary heart disease, atherosclerosis, stroke [14, 16, 18]. The causes of HHC are usually genetic defects of enzymes of homocysteine metabolism (methylenetetrahydrofolate reductase, cystathionine-?synthase, methionine synthase), deficiency of vitamins B6, B9, B12, renal failure, alcoholism, etc. Under these conditions, it is not utilized by transsulfuration and remethylation reactions and accumulates in cells and blood plasma. In the cells of various organs, it causes damage to disulfide bonds
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