The purpose of the research was to study the effect of gestational age on the state of the enzymatic link of antioxidant protection (AOP) of lipid peroxidation products (LPO) in cows with anemia syndrome and chronic systemic inflammation. Three (3) groups of cows were formed: group I (n=15) – healthy; group II (n=8) – with hypochromic microcytic anemia; group III (n=7) – with chronic systemic inflammation syndrome of low intensity. On days 150-160, 210-220 and 260-265 of gestation, blood samples were taken to study the indicators of LPO, AOP and endogenous intoxication. There were obtained the data on the peculiarities of the state of the LPO-AOP system in cows with various clinical states during gestation. It has been established that there is an inverse correlation between the period of gestation and catalase activity. A significant direct correlation of high strength with respect to the level of nitric oxide has also been revealed. In cows with anemia, less intense tendencies for an increase in nitric oxide have been noted, which may have an important role in the control of fetoplacental hemodynamics and saturation of the fetal blood with oxygen. In group I and II, the level of diene conjugates had a significant direct correlation of noticeable strength, but in group III, the binding strength increased and became high, which was reflected at the level of molecules of average molecular weight, detectable at a wavelength of 254 nm. Thus, with an increase in the duration of gestation, there is an increase in the LPO intensity, which is most pronounced in cows with a syndrome of chronic systemic inflammation of a low degree of intensity, as a result of which endogenous intoxication develops. At the same time, nitric oxide is less actively produced in cows with anemia that can lead to the development of fetoplacental insufficiency and hypoxic state of the fetus.

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.

The article presents the results of a study of the potential mutagenic effects of the drug Interamin on the bone marrow of mice. Its effect on the cytogenetic stability of bone marrow cells after injection of an experimental mutagen (mitomycin C) was also studied. The antimutagenic potential of Interamin was studied relative to the reference drugs Aminoseleton and Bifeton-B. The study of the mutagenic effect of the compounds was carried out using a micronucleus test in polychromatophilic erythrocytes of the bone marrow of mice that is an assessment of the change in the frequency of micronuclei in polychromatophilic erythrocytes. The toxic effect of drugs on bone marrow cells was assessed by the change in the proportion of polychromatophilic erythrocytes relative to the number of normochromic erythrocytes. As a result of the study, no changes were found in the frequency of micronuclei in polychromatophilic erythrocytes and the percentage of cells of this type in the bone marrow of mice treated with Interamin at a conditional therapeutic and tenfold increased doses, as well as with its fivefold administration at intervals of 24 hours at a conditionally therapeutic dose. The course use of the study drugs at a therapeutic dose before the administration of mitomycin C led to a decrease in the frequency of micronuclei in polychromatophilic erythrocytes by 39.1% (p=0.002) and 47.6% (p=0.009) when using Interamin and Aminoseleton, respectively, relative to the indicators of animals, who were administered only mitomycin C. In the group treated with Biferon-B, such trend was not observed. At the same time, in animals of these groups, the proportion of polychromatophilic erythrocytes was higher by 33.3% (p=0.002) after the administration of Interamin and by 57.2% (p=0.009) after the use of Biferon-B, relative to the animals of the positive control group. The presented data indicate that the drug Interamin has no mutagenic properties, as well as the presence of antimutagenic and antitoxic effects that opens up prospects for its use as a gene protector and antitoxicant.

The aim of this work was to study the antimutagenic and DNA-protective effects of lipophilic cryofractions of bovine spleen and placenta in mice with mitomycin (MM)-induced genotoxicity. The effect of lipophilic cryofraction of bovine spleen (LCSC), lipophilic cryofraction of bovine placenta (LCPC) and their mixture in equal proportions (LCSPC) was studied. Outbred male mice were used in the experiments. The effects of a single administration of the substances separately and simultaneously with an intraperitoneal injection of MM were studied, as well as with three-time administration of the substances with an interval of 24 hours before the administration of MM relative to the negative and positive control groups. Afterwards, bone marrow samples were obtained from the animals for the micronucleus test and liver samples to determine the amount of mitochondrial DNA (mtDNA) damage in the 12S-16S and ND5 fragments. A single administration of LCSC, LCPC and LCSPC reduced the frequency of polychromatophilic erythrocytes with micronuclei (MNPCE) by 4.1, 3.9 and 2.4 times (p < 0.05), respectively, relative to the positive control group mice. With a course of administration of LCSPC, the frequency of MNPCE decreased by 31.3% (p < 0.05) relative to the positive control group. Administration of LCSC and LCSPC reduced the amount of mtDNA damage by 96.5 and 68.3% (p < 0.05), respectively, in the 12S-16S fragment relative to the positive control group mice. A course of administration of LCSPC before MM reduced the amount of mtDNA damage by 52.2% (p < 0.05) in the ND5 fragment. The antimutagenic effect of the studied cryofractions and the DNA-protective effect of LCSC and LCSPC in relation to mtDNA were revealed.

This research was aimed at studying the effect of species-specific recombinant bovine interferon lambda (IFN-λ) on the generation of reactive oxygen species (ROS) in mouse liver and bone marrow cells under conditions of mitomycin Cinduced oxidative stress. The experiment included female white laboratory mice. There were formed four groups of 6 animals each: the negative control group (group I); the group of mice that received a three-fold injection of IFN-λ at a dose of 0.1 ml/kg (group II) and mice that, in addition to IFN-λ, were administered a cytotoxic drug that induced free radical oxidation processes - mitomycin C at a dose of 10 mg/kg (group III), as well as the animals receiving only mitomycin C (group IV). We studied the concentration and viability of a cell suspension obtained from the liver of mice, as well as the relative content of intracellular ROS in the liver and bone marrow cells of animals, assessed by the fluorescence intensity of the oxidized form of 2',7'-dichlorodihydrofluorescein diacetate. The concentration and viability of cells in the liver suspension of healthy mice did not change with the introduction of IFN-λ (group II), indicating the absence of a toxic effect of IFN-λ on these cells. An increase in the level of ROS in the studied cells was detected when IFN-λ was administered to mice of group II (an increase in the level of ROS by 1.3 times in liver cells and by 2.9 times in bone marrow cells, relative to the mice of group I) and a decrease in the level of ROS in the mice under conditions of oxidative stress induced by mitomycin C (reduction in the content of intracellular ROS by 1.9 and 7.2 times in liver and bone marrow cells in the animals of group III, relative to the mice of group IV). The presented changes may indicate the normalization of IFN-λ redox balance in the body and, probably, appear in connection with the immunomodulatory activity of IFN-λ.