Abstract:
Homocysteine (Hc), a product of methionine metabolism, can negatively affect internal organs' structural and functionalparameters, including the spleen. The study aims to study the microscopic changes in the spleen of adults and old rats underconditions of chronic hyperhomocysteinemia (HHc). Experiments were performed on 44 white male rats (adult rats aged 6-8 monthsand old rats aged 24-26 months). The animals were divided into control and experimental groups (11 individuals in each group) duringthe experiment. Chronic HHc was achieved by administering D, L-thiolactone homocysteine hydrochloride to experimental groupanimals at a dose of 200 mg/kg of body weight intragastrically (intravenously) in a 1% starch gel solution once a day for eight weeks. After the end of the experimental simulation of chronic hyperhomocysteinemia, the animals were removed from the experiment byanaesthetising by decapitation and using thiopental anaesthesia. Histological preparations were studied using an SEO SСAN lightmicroscope. It was found that under conditions of chronic HHc in adult rats, densification and disorganisation of the fibres of the denseconnective tissue of the capsule and trabeculae of the spleen, vacuolisation of the cytoplasm of endotheliocytes of large-diametervessels were noted. T-cells of the white pulp were subject to death by apoptosis, and B-cells of lymphoid nodules and marginal zonesshowed signs of marked proliferation. Modelling persistent GHz in old rats led to changes in the spleen's stromal and parenchymalstructural elements. The capsule of the organ lost the clarity of its contours and was blurred and thickened. Lightening zonescharacterised periarterial sheaths due to the massive death of T-lymphocytes. The number of bright germinal centres and plasmacells increased. The number of macrophages containing lipofuscin inclusions increased in the red pulp. All these changes werecaused by the irritating effect of excessive doses of homocysteine, particularly oxidative stress and nitrosylation, which suppressesthe mechanisms of cell adaptation to this stress and hypomethylation of cell DNA.
