Abstract
The influence of selenolin on the metabolic functions of the liver of laboratory rats was studied on the model of the reproduction of acute liver failure caused by acetaminophen. It was determined that the use of selenolin inhibits and weakens the hepatotoxic effects, contributing to the correction of impaired homeostasis in rats. Under the action of the preparation, there was a decrease in enzymatic activity – AST – in 2.35 times, ALT – in 2.4 times, γ-GGT – by 21.7%, as well as an improvement in protein synthesizing function, manifested by an increase in the concentration of total protein by 26.9%. Selenolin significantly (p <0.05) reduces the level of lipid peroxidation products – DC – in 1.5 times, CD – by 56.3%, MDA – by 19.9%. Due to the organic selenium included in the preparation, selenolin helps to maintain a high activity of the enzyme antioxidant system, which leads to a decrease in the stationary level of free radical and lipid peroxidation products, allowing the body to quickly cope with pathological changes in the liver cells and in the blood homeostasis system.
Highlights
The purpose of studying the specific activity of drugs is to conduct pathophysiological experiments that allow reproducing models of acute and chronic diseases in laboratory animals, and using these models, to identify the patterns of their development, starting from the moment the etiological factor interacts with the body until the outcome
In the mechanisms of development of liver diseases, one of the essential features is the activation of lipid peroxidation (LPO) processes, leading to damage of hepatocytes at the membrane level [5]
When using high doses of the drug, these mechanisms are saturated and paracetamol begins to metabolize in the cytochrome P-450 system with the formation of a toxic metabolite –N-acetyl-p-benzoquinone imine (NAPQI), which has direct damaging effects on hepatocytes: disturbance of calcium flow in mitochondria, formation of hydroxyl radicals, formation of nitrites and nitrates that leads to the activation of apoptosis
Summary
The purpose of studying the specific activity of drugs is to conduct pathophysiological experiments that allow reproducing models of acute and chronic diseases in laboratory animals, and using these models, to identify the patterns of their development, starting from the moment the etiological factor (toxicant) interacts with the body until the outcome. It is possible to determine the relationship between damage and the functional state of various organs, systems and the body as a whole [1, 2]. The means of metabolic therapy of liver diseases include all substances that have hepatoprotective activity, including the pronounced antioxidant effect and potentiation of endogenous antioxidant systems of hepatocytes, inhibition of phospholipolysis with a decrease in the production of lysophosphatides and restoration of the normal spectrum of membrane phospholipids, deposition of calcium ions, as well as improvement matrix and barrier functions of cytolemma, mitochondrial membranes, endoplasmic reticulum (EPR) and lysosomes [3, 4]. In the mechanisms of development of liver diseases, one of the essential features is the activation of lipid peroxidation (LPO) processes, leading to damage of hepatocytes at the membrane level [5]. Under conditions of the liver pathology, the intensity of LPO depends on many factors, correlating both with the activity of the pathological process and with the functional state of the antioxidant system of hepatocytes. The main role in the destruction of unsaturated fatty acid hydroperoxides formed during LPO plays the glutathione system, in particular, glutathione peroxidase – glutathione reductase
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