Histological and histochemical changes in liver tissue of young rats with hyperhomocysteinemia

Abstract

The decisive place in the synthesis and subsequent metabolism of homocysteine (Hcy) belongs to the liver, where, inparticular, transsulfation and remethylation processes take place. It has been proven that organ tissue damage can cause hyperhomocysteinemia (HHcy). Changes in the structural and functional parameters of the liver tissue under the conditions of asignificant and long-term increase in blood serum Hcy are still insufficiently studied. Modeling the state of chronic HHcy and studyingthe features of histological changes in liver tissue at different levels of structural organization is an urgent task. The aim of theresearch is to study morphological and histochemical changes in the liver tissue of young rats with HHcy. The experiment was carriedout on 22 white non-linear young - aged 1-2 months, male rats. During the study, the animals were divided into two groups - control andexperimental. Chronic persistent HHcy was modeled by administering thiolactone Hcy in a dose of 200 mg/kg of body weightintragastrically for 60 days to the rats of the experimental group. Histological preparations were studied using a SEO SСAN lightmicroscope and photo-documented using a Vision CCD Camera. Succinate dehydrogenase was detected histochemically accordingto the Nakhlas method. To study the specifics of glycogen accumulation in hepatocytes, sections were stained using Schiff's reagent,after preliminary treatment with iodic acid (PAS reaction) in the Shabadash modification. It was established that the administration ofthiolactone Hcy to young rats at a dose of 200 mg/kg led to impaired blood supply, destructive changes and growth of connective tissuein the liver. Moderate changes in the hepatocyte plates organization, a decrease in the mitotic activity of hepatocytes, and thedevelopment of fatty and vacuole-hydropic dystrophy were recorded. Histochemical studies of the liver of animals of the research groupestablished a decrease in the activity of the succinate dehydrogenase enzyme and glycogen content in hepatocytes.