THE INFLUENCE OF EXOGENOUS XENOBIOTICS ON ADSORPTION OF IRON IONS AND HEMATOPOIESIS

Abstract

An acute hepatotoxic liver injury by administering a single peritoneal bolus injection of thioacetamide causes an imbalance between the synthesis and degradation of proteins in the extracellular matrix and is a trigger of fibrogenesis. In the scientific publications, the intoxicationtriggered changes are described using the changes with time in proinflammatory and profibrotic cytokines, without considering hematological indices. The aim of the study was to establish the nature of morphometric changes in hematological parameters caused by a prolonged toxicity of thioacetamide and ethanol. The results of the study. It has been noted that changes in RBC indices in the group of test animals consisted in an insignificant reduction in absolute counts of red blood cells and mean corpuscular volume while maintaining the homogeneity of the population, as suggested by slight fluctuations of such indices as RDW-SV, which in the test group increased significantly (p˂0.05) by 4.38%, and RDV-CV, which decreased by 0.71%. Activation of megakaryocytic cells was detected, as evidenced by a significant (p˂0.05) 28.21% increase in immature platelet counts (P-LCC) in the group of test animals and a 22.54% increase in large platelets P-LCR fraction compared with the finding in the group of intact animals. The hepatotoxic effect of thioacetamide, a hydrophilic xenobiotic, was shown to cause changes in iron adsorption, which consisted in a significant (p˂0.05) 28.07% ferritin increase in the test group against the background of a 17.68% reduction in plasma levels of Fe+3 ions in the animals compared to controls. The reduction in Fe+3 stores in plasma as a result of its deposition as ferritin is leading to a reduction in volume fraction of RBCs in whole blood, as suggested by a 12.23% hematocrit reduction in the group of test animals. Prolonged intoxication by exogenous xenobiotics for 21 days caused the development of inflammation, as suggested by the increased concentration of C-reactive protein (up to 1.67 mg/dl*10-2) and corresponding to its significant increase by 23.35% compared to controls. The development of the inflammation involved the population of neutrophils and lymphocytes, the absolute counts of which increased significantly in the test group (p˂0.05): by 58.73% and by 46.28%, respectively.