Prophylactic stimulation of protective liver function in rats against the background of experimental aflatoxicosis

Mycotoxicosis continues to be an urgent problem in the agricultural sector, as mycotoxins are widespread as contaminants in feed and food products. The mold fungus of the genus Aspergillus secretes several types of aflatoxins (B1, B2, G1 and G2), of which aflatoxin B1 belongs to the group of particularly dangerous. Aflatoxin B1 exhibits tropism to hepatocytes, destabilizing the processes of metabolism and detoxification in the organ, and the development of pathological changes at the macro- and microscopic levels disrupts the basic functions of the liver, which in turn induces multiple organ failure. The purpose of this work is to study the effect of the preventive agent «Hepatoprotect» developed on the basis of the FSBSI «FCTRBS-ARRVI» on the preservation of the rat hepatocytes morphology in conditions of experimental aflatoxicosis. The object of the study was white rats, which were divided into 3 groups (6 heads each) according to the principle of analogues, taking into account weight, gender and age. The first group served as the biological control of the experiment. The second was a toxic control that received aflatoxin B1 with food. The third group was simultaneously given food contaminated with aflatoxin B1 and the «Hepatoprotect» dietary supplement. After euthanasia, liver samples were taken, which were examined at the histological and ultrastructural levels. The results of the histological examination demonstrated the positive effect of the feed additive «Hepatoproject» on the preservation of the rat liver histoarchitectonics in conditions of experimental aflatoxicosis. Based on the data of the ultrastructural study and their statistical processing, the protective effect of the feed additive «Hepatoprotect» against the mitochondria of white rat hepatocytes was also confirmed. The developed means of preventing mycotoxicosis contributes to the maintenance of cellular respiration processes, reducing the risk of hypoxia, leading to the mass death of hepatocytes.