Формування ультраструктурних адаптивних реакцій у тканинах організму при експериментальному паркінсонізмі

Abstract

We studied changes in the ultrastructure of brain tissues - medulla oblongata and striatum, as well as lung and heart tissues in experimental parkinsonism caused by the action of rotenone, which was administered once or for 2 weeks. It has been shown that during the development of a Parkinson-like state the ultrastructure of tissues disturbance, the development of mitochondrial and endothelial dysfunction is observed not only in parts of the brain, but also in other tissues of the body. Mitochondrial dysfunction is significantly expressed in the medulla oblongata, as evidenced by, firstly, a decrease in the total number of mitochondria by 35.7%, and secondly, damage to their ultrastructure in more than 40% of organelles. Endothelial dysfunction was indicated by hyperhydration of the blood-brain barrier. In the tissue of the striatum, the indicated changes were insignificant, instead, a compensatory restoration of dynamic processes in the mitochondrial apparatus, in particular fission-fusion processes, was observed. In the myocardium, there were also significant changes in the ultrastructure, this indicated the development of both mitochondrial and endothelial dysfunctions. As well as in the medulla oblongata tissue, about 40% of mitochondria were found to be damaged, although it should be noted that although not pronounced, but still reliable (by 12.6%) activation of mitochondrial morphogenesis was observed. The histohematal barrier, in particular its endothelial layer, thinned due to destructive processes. Violations of the ultrastructure were also observed in the lung tissue. Significant changes in the mitochondrial apparatus with damage to the mitochondrial structure were revealed. However, the percentage of structurally damaged organelles was significantly (almost 2 times) lower than in the myocardium (reached only 25%). The thickness of the endothelial layer of the air barrier increased by an average of 30%. In tissues where mitochondrial and endothelial dysfunction were less pronounced during longterm administration of rotenone, adaptive changes begin to form, which are probably also observed in people with Parkinson’s disease, which enables them to adapt to the existing disease.