Structure of a liver in the conditions of chronic influence of sodium tetraborate

Abstract

Introduction. One of the target organs of xenobiotics is the liver, wherein severe impairments of tissue structure developed under the influence of toxic substances, which manifest as dystrophy, bloodstream widening, and hepatocyte regeneration disorder. Liver as the biggest gland in the organism, receives double blood irrigation enriched with oxygen by its own hepatic artery and nutrient – rich from the portal vein being the first organ that receives metabolic substrates and nutrients from food. Therefore, the liver is constantly exposed to toxic substances that are absorbed, degrade, and conjugate. Goal of research is to study the influence of tetraborate sodium on liver structure. Methods. Chronic impact of sodium tetraborate on structure of a liver of white, not purebred rats – males was studied. Research was conducted on 30 puberal rats (10 intact, 10 control, 10 experimental). Sodium tetraborate was administered to the experimental animals within 2 months intraventricularly in a dose of 150mg/kg (1/30 LD50). After histologic diagnosis paraffin sections of a liver were stained with hematoxylin and eosine and according to Van Gieson. Results. At chronic poisoning with sodium tetraborate the blood stasis - filling with blood of the central vein of a hepatic segment, expansion of sine capillaries, overfilling with blood of interlobular veins were observed. The degenerated cells (12,3±1,24%) were observed, generally round the central vein.They did not occur in intact and control animals. The number of two-nuclear cells was increased to 12,7±1,75% (in control 5,8±0,41, %). There was an increase in the polyploid cells, if in the control they made 2,2±0,12%, then in experiment their quantity reached 4,3±0,27%. Conclusion. The toxic effect of borax induces degeneration of hepatocytes. The toxic substance effect produces an inflammatory process, accompanied by intensified exudation and formation of a large amount of tissue fluid, which induces circulatory dynamics imbalance. The morphofunctional deficiency, induced by cell death, causes proliferative processes in the form of an increasing number of double nucleated and polyploid hepatocytes.