The purpose of the work was to explore the indicators of functional state and function of protein synthesis of the cow liver within experimental fasciolysis, sensitized to atypical mycobacteria. Ten cows of black-and-white breed were selected for the experiments. Two groups consisting of five animals each were formed. The control group cows were clinically healthy. The animals of the experimental group were contaminated with mycobacteriosis and fascicular invasion. In the course of research, the rules for performing zootechnical experiments on the selection and maintenance of animal-analogues in the group, harvesting technology, use and accounting of consumed feed were followed. Being impacted by fascicular invasion, the cattle sensitized with mycobacteria demonstrated the suppression of the liver protein synthesis function, which manifests itself as a decrease in total blood protein, a decrease in the level of albumins and an increase in the level of globulins. According to the clinical manifestation of fasciolosis in the cattle sensitized with atypical mycobacteria, disease pathogens have a toxic effect on hepatocytes causing an increase in the permeability of the biological membranes of the cell membranes. The indicated changes lead to an increase in the activity of blood serum enzymes, in particular, aminotransferases (AsAT and AlAT) and alkaline phosphatase. High activity of AlAT and AsAT in the blood serum of the cows under experimental fasciolysis sensitized by atypical mycobacteria, indicates destructive processes in the liver that cause release of aminotransaminases from cellular organelles in the blood of the cattle. Thus, the results obtained indicate an increase in destructive processes in the body of the cows under experimental fascioliasis sensitized with atypical mycobacteria.
The work reveals the immunobiological aspects of lactation of cows and changes in immunobiological reactivity in the development of mastitis.The authors present modern scientific data on the local immune protection of the mammary gland of cows. Main stages of ontogenetic development of cellular immunity of the mammary gland of cows were traced during clinical and experimental studies. The number of somatic cells in the secret of the mammary gland of the primates was dependent on the period of the functioning of the mammary gland. In the cytology of colostrum mostly (56.00 ± 1.90%) neutrophil granulocytes were predominant, in the middle period of lactation (3–5th month) the proportion of epithelial cells increased (from 29.51 ± 2.17 to 49.59 ± 1.94%), during the launch period, the population of polymorphonuclear neutrophil granulocytes was changing as well, which virtually recovered to the original level and increased during the dry period. However, at the end of lactation, during the onset and dry, with the development of involutionary processes in the mammary gland, a sharp decrease in cytochemical reactivity of intracellular lysozyme of phagocytic cells was observed. To conduct clinical and experimental studies, three groups of animals were formed. As a result, it was found out that subclinical mastitis of cows is accompanied by a change in the immunobiological reactivity. Purulent-catarrhal mastitis in cows was manifested by significant changes in the parameters of nonspecific immunological reactivity. In the peripheral blood of cows with subclinical mastitis, the number of reactive microphages increased sharply (P < 0.001). In parallel with this, the number of activated phagocytes with myeloperoxidase granules also increased in the peripheral blood (P < 0.01). Activation of intra-leukocyte lysozyme phagocytic cells was less intensive. Subclinical udder pathology was accompanied by an increase in the number of degranulated cells (P < 0.001), which is one of the specific properties of cytomorphological changes in programmed death (apoptosis). Subclinical inflammation of the mammary glands mastitis of cows was accompanied by a certain decrease in the number of T-lymphocytes (P < 0.001). Clinical and experimental studies have shown that subclinical and purulent-catarrhal mastitis of cows undergo significant changes in systemic immunity. In the pathophysiological model of subclinical and purulent-catarrhal mastitis, the functional state of the T-link of specific immunity was disturbed, the bactericidal activity of blood serum and phagocytosis were suppressed, which occurred against the background of changes in the cytochemical reactivity of phagocytic cells circulating immune complexes and molecules with an average molecular weigh.
Science is constantly evolving and updated with current data on cell biology. The cellular aging phenomenon should be considered an evolutionary mechanism of the biological regulation of all living organisms. Factors initiating cellular aging are variable. Each cell type can respond differently to the activation factors of cellular aging. In recent decades, science has been supplemented with new data that provide a deeper understanding of cellular and molecular mechanisms of cellular aging and the formation of immune homeostasis. There is a real prospect of using effective means of its regulation. In recent years, scientists have come close to discovering the mechanisms of cellular aging. Factors and mechanisms of cell regeneration are more deeply revealed. Scientists are also better aware of the phylogeny and ontogenesis of immune processes and the role of immune factors in developing pathologies. Researchers are increasingly focusing on modern diagnostic methods and xenotherapy. However, the specific factors of immunoregulation and the interaction of microphages, macrophages, and lymphocytes with other body cells are not yet fully understood. Accordingly, this requires further in-depth study. This review reviews the current literature on cellular aging and its regulatory mechanisms. The authors also present the results of their research on the mechanisms of immune responses in reproductive pathology. They draw parallels with modern scientific theories and interpret research. We will also focus on the issues that need to be addressed in the near future for the progressive development of this field of science. Thus, the study of the mechanisms of cellular aging and the development of effective means of hay therapy today requires further painstaking work. Despite significant advances in preclinical studies, many questions remain about the practical use of the drugs. This is especially true in the medicine of oncology, neurology, and cardiology. Nevertheless, scientists will be able to use pharmacological agents to influence cell division, differentiation, and determination in the future. We also hope to have developed effective means of immunotherapy of diseases. The molecular mechanisms of cell aging and mediators involved in the mechanisms of cell aging and death are being studied in detail. The field of research contains countless fascinating studies that are sure to be discovered.
Since the middle of the last century, scientists have been interested in the mechanisms of regulation of cell division, differentiation and aging of cells. The first objects of study were insects, helminths and other living organisms. From the very beginning, in the biology of cell development and regulation, scientists have attached leading importance to genetic factors. Later, more and more experience was gained on the influence of intracellular factors, metabolic changes and exogenous pathogens on the programmed cell death. Recent research on cell biology and pathology has focused on the study of apoptosis. The first described phenomenon of programmed cell death was apoptosis. Subsequent studies were aimed at the study programmed cell death. This review will provide an opportunity to consider the biological mechanisms of programmed cell death, differences and species characteristics. The author described the clinical aspects of apoptosis, necroptosis and pyroptosis and their importance in the formation of cellular homeostasis. In the present review article simple classification system, where the cell death entities are primarily categorized into programmed cell death. Multiple mechanisms and phenotypes compose programmed non-apoptotic cell death, including: autophagy, entosis, methuosis and paraptosis, mitoptosis and parthanatos, ferroptosis, pyroptosis NETosis and necroptosis. Changes of cellular regulation at development of pathologies at people and animals are considered. Cell biology includes a variety of mechanisms of programmed aging and death. Modern research is aimed at deepening the study multiple mechanisms and phenotypes compose programmed. Cells. will certainly be taken into account by the Nomenclature Committee on Cell Death. Cellular regulation is associated with a variety of physiological mechanisms of development, and is also important in processes such as inflammation, immune response, embryogenesis maintenance of tissue homeostasis. Study of factors of influence and mechanisms of regulation of aging of cells opens a curtain for development of the newest means of diagnostics of pathologies and development of pharmacological means for correction of cellular mechanisms at development of pathologies.
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