The article provides an overview of the most significant works of domestic and foreign authors devoted to the Ehrlich ascites carcinoma biological model. The analysis of the available literary sources showed that despite the long history of the existence of this model and its application in biomedical research, it has not yet become widespread in veterinary medicine. It should be noted that the Ehrlich ascites carcinoma model has a number of peculiarities that allow it to be used for the needs of veterinary medicine, in particular, experimental pharmacology at the stage of drug design and its preclinical testing. The high resistance of malignant cells and tumor survival in experimental animals, as well as the ease of its cultivation and relatively rapid tumor growth, make this model a convenient biological object for research. The effect of tumor cells on the body of the animal with a tumor leads to a change in a number of biochemical indicators of various tissues and organs, and a general toxic effect. In this case, an imbalance of the free-radical and antioxidant systems is observed, the body is exposed to oxidative stress. The immune system under the effect of Ehrlich ascites carcinoma also undergoes a number of changes. Thus, in response to the development of tumor-induced pathological processes, recruitment of immunocompetent cells and an antitumor immune response are observed, which at the same time is suppressed as carcinoma cells grow under the action of immunosuppressive physiologically active compounds produced by the tumor, escape of tumor cells from immunological surveillance and remodelling of immune cells in the tumor microenvironment. These processes lead to suppression of the immune system and as a result to the death of animals. These peculiarities make it possible to use the Ehrlich transplantable ascites carcinoma model for testing new veterinary drugs with potential antiblastoma, immunomodulatory, antitoxic properties, as well as medicinal formulations for restoring biochemical indicators and redox homeostasis under conditions of tumor-induced immunosuppression and chronic inflammatory process, and also to study the mechanisms of cell adaptation, including the immune system, under the action of carcinogenesis factors.
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