Abstract

Thyroxine and Triiodothyronine are very important for normal growth, development and organ function. These hormones regulate the basal rate of metabolism of all cells, including hepatocytes, and thus modulate liver function. There is a close connection between hyperhomocysteinemia (HHCy) and the induction of oxidative processes, disruption of nitric oxide production of NO synthase, damage to the endoplasmic reticulum and activation of inflammatory processes in the liver. Disorders of homocysteine metabolism (HC) in thyroid dysfunction are also known. Therefore, it can be assumed that the violation of the structure and functions of the liver will be an important manifestation of the negative impact of HHCy on organs and tissues in hyper- and hypothyroidism. The aim of the study was to establish the reorganization of the structural components of the liver in the conditions of modelized HHCy, hyper- and hypothyroidism and their joint effects. Thiolactone HHCy was modelized by administering to animals an exogenous HC in the form of Thiolactone at a dose of 100 mg/kg body weight once a day for 28 days. Hyperthyroidism was modelized by daily administration of L-thyroxine at a dose of 200 μg/kg for the 21 days, hypothyroidism - daily administration of Thiamazole at a dose of 10 mg/kg for the 21 days. Individual groups of animals were administered L-thyroxine and Thiamazole in parallel with HC. It was found that in the conditions of simulated HHCy, hypo- and hyperthyroidism in the liver of experimental animals there is an incompleteness of hepatocyte beams, changes in hepatocytes of destructive, dystrophic and necrotic nature with signs of steatosis, vascular disorders. Conclusions: both HHCy and hypo- or hyperthyroidism lead to a violation of the structural organization of liver tissue. With the development of thyroid dysfunction on the background of HHCy, the disturbances of the histological structure of hepatocytes significantly increased.

Highlights

  • Thyroxine and triiodothyronine are necessary for normal growth, development and functioning of organs

  • Cirrhosis of the liver in humans is known to be associated with HC metabolism, in particular the expression of methionine synthase, betaine

  • We have shown that the experimental reproduction of hyperthyroidism leads to a decrease in the level of HC, and hypothyroidism, in contrast, causes an increase in the content of HC in the blood, which is associated with changes in the activity of methionine and cysteine [15]

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Summary

Introduction

Thyroxine and triiodothyronine are necessary for normal growth, development and functioning of organs. These hormones regulate the rate of basic metabolism of all cells, including hepatocytes, and modulate liver function; the liver in turn metabolizes thyroid hormones and regulates their systemic endocrine effect. Mechanisms associated with disorders of sulfurcontaining amino acid metabolism are known to play a significant role in the development of liver pathology. A special role in the synthesis and metabolism of the latter is assigned to the liver, in which a significant part of transmethylation reactions occurs [17]. Elevated levels of HC in the blood can cause liver damage and, liver damage often leads to disorders of HC metabolism. Cirrhosis of the liver in humans is known to be associated with HC metabolism, in particular the expression of methionine synthase, betaine-

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