CLINICAL-BIOCHEMICAL CHANGES OF RAT'S BLOOD WITH MODELED GALACTOSAMINE HEPATITIS ON THE BACKGROUND OF MERCAZOLILUM-INDUCED HYPOTHERAPY

Abstract

Today, thyroid disease in its prevalence occupies one of the first places among endocrine pathologies in many countries. Thyroid hormones regulate the level of basal metabolism of all cells, including hepatocytes, which affects the functioning of the liver, and the liver, in turn, metabolizes thyroid stimulating hormone (TSH). Disorders of thyroid function may lead to changes in liver function, and in liver disease, there may be a deviation in the metabolism of TSH. The liver has a central role in the dehydration of TSH with the formation of their active or inactivated forms. The deficiency of thyroid hormones in the body leads to a violation of the water-electrolyte, protein, lipid, carbohydrate metabolism, causing morpho-functional and biochemical changes in various organs and systems.

The aim of the study – to learn the dynamics of changes in biochemical parameters in the blood and liver tissue of rats with acute hepatitis against mercazolilum-induced hypothyroidism.

Materials and Methods. In this paper, a study is made of the dynamics of changes in biochemical parameters in blood and liver tissue of rats with acute hepatitis against the background of mercazolilum-induced hypothyroidism. Proceeding from this, hypothyroidism was simulated by daily administration of per os by means of a special probe of pharmacopeial thyreostatics of mercazolilum. Control was performed on the level of thyroxine, triiodothyronine and thyroid stimulating hormone, as well as the weight of animals and their motor activity. The comparison group included animals that Mercazolil was not administered. Influence of hypothyroidism on the course of inflammatory process in the liver was studied on the model of galactosamine hepatitis, which was induced by intraperitoneal administration to the experimental animals of galactosamine. In the 1 st and 7 th day after the modeling of hepatitis, the rats were decapitated under thiopental anesthesia.

Results and Discussion. In the experiment on rats, the peculiarities of the dynamics of biochemical parameters in the blood and liver homogenate were studied in the case of simulated galactosamine hepatitis against the background of hypothyroidism. It was found that toxic liver damage in rats is accompanied by the activation of the systemic response of the local inflammatory reaction, an increase in the content of active neutrophils in the peripheral blood caused by the intensification of nonspecific factors of immune defense, reduction of reserve parameters and biochemical parameters of the thiol-disulphide system.

Conclusions. In rats with simulated hypothyroidism, there was a decrease in the indicators of the glutathione chain of the thiol-disulfide system, namely glutathione peroxidase (GP), glutathione reductase (GR) and indicators of reductive glutathione. Also, there was found an increased score of CNST and INF. In acute galactosamine hepatitis, a decrease in the indicators of the glutathione chain of the thiol-disulfide system, namely, glutathione peroxidase (GP), glutathione reductase (GR) and reductive glutathione, has been found, and an increased score for cHCNT and hNST has been found. In experimental galactosamine hepatitis on the background of hypothyroidism, we observed similar changes.