The possibility of induction of cytogenetic damage in the bone marrow, changes in the cellularity of lymphoid organs and blood composition in mice irradiated with low-intensity femtosecond laser radiation at a power flux density of 5.1, 10.4, and 52 mJ/cm2 (0.5 mW for 5, 10, and 50 s) in vivo was shown. Using the radiation adaptive response test (0.1 Gy + 1.5 Gy), it was found that, when mice were exposed to femtosecond laser radiation in high doses, the body’s natural defenses were activated in the same narrow range of energy flux density (2–16 mJ/cm2) as in the case of X-ray irradiation in a dose of 0.1 Gy (4 mJ/cm2). The data obtained suggest a similar mechanism of activation of the body’s natural defense upon exposure to low doses of both ionizing and non-ionizing radiation.

We studied the effect of different concentrations of polyelectrolytes poly(allylamine hydrochloride) (PAH) and polystyrene sulfonate (PSS) as well as the effects of microcapsules coated with these polymers on survival of Ehrlich ascites carcinoma cells and mouse peritoneal macrophages and on ROS production by phagocytes. PAH reduced viability of Ehrlich ascites carcinoma in a concentration-dependent manner (LD50=12-15 μg/ml). This effect was presumably determined by its ability to bind phosphates, thereby depleting the culture medium. At the same time, PAH did not affect the viability of macrophages. PSS produced no cytotoxic effect on the examined cells. Polyelectrolyte capsules with the shell architectonics (PAH/PSS)3 and (PAH/PSS)3PAH in the examined concentration range had no effect on the viability of macrophages and tumor cells. PAH microcapsules with positively charged surface much more rapidly and more intensively activated macrophages. The chemiluminescence response directly depended on the amount of capsules in the solution.

Relationship between changes in the erythrocyte sedimentation rate in rats and concentration and charge of polyelectrolyte microcapsules was studied by the Panchenkov method. Positively charged microcapsules reduced erythrocyte sedimentation rate in a concentrationdependent manner. This effect was related to a decrease in the content of high-molecularweight proteins in the plasma due to their adsorption in positively charged microcapsules with polyacrylamide surface layer.

In this work, the effect of tumor growth on the antioxidant system was studied in blood plasma and the tumor growth zone. As a model system of tumor growth, we used Zajdela ascitic hepatoma transplanted into the abdominal cavity of Wistar rats. The tumor produced a disbalance between pro- and antioxidant systems in the body of the tumor bearer. In the blood plasma, a sharp fall of tocopherol and uric acid concentrations (by two times), as well as of protein SH-groups (seven times), was found. In the tumor growth zone, alongside with a decrease of the tocopherol level, a five- to sevenfold increase in uric-acid concentration and in protein SH-groups was noted. With decreasing concentration of low-molecular antioxidants, the key role begins to be played by the protein components that bind or oxidize ions of metals of variable valence. Thus, the level of transferrin (Tf) responsible for transporting iron ions in the blood plasma during tumor development decreases 2.5–3 times (from 5.0 to 1.6 mg/mL), whereas, in ascitic fluid, a Tf increase is observed of from 1.5 to 2.7 mg/mL. The concentration dynamics of another protein—ceruloplasmin (Cp)—functioning together with Tf has opposite tendencies. Thus, in the blood plasma, the Cp concentration increases 1.5–2 times (from 0.55 to 1.1 mg/ml), whereas in the ascitis it decreases from 0.55 to 0.35 mg/mL.

The modern problems associated with the life quality and duration of oncologic patients must be solved by refining the methods of diagnostics and efficient therapy. To do this, we have to know the mechanisms of processes that accompany neoplasm development. The purpose of our study was to determine marker parameters associated with production of NO in the blood and in the area of tumor growth, in order to reliably separate the process of ascites tumor development into individual differentiated stages. Zeidel ascites hepatoma transplanted into Vistar rat abdominal cavity was used as a model of tumor development. It was found that the tumor causes the development nitrosative stress in the blood plasma and its manifestations in the course of tumor growth being different. Thus, in the early stages of tumor growth, a marked accumulation of protein modification products was observed. The first phase is showing for the most part accumulation of nitrotyrosine and phase 2 accumulating mainly S-nitrosothiols. The therminal stage was characterized by increased concentrations of nitrites/nitrates. Modified proteins fall in ascites with a current fluid of ascites tumors differentiated into separate stages on the example of a model tumor hepatoma Zeidel.

The influence of nitric oxide (NO) donor, NO-synthase substrate (L-arginine), and inhibitor (nitroarginine) on the reactive oxygen species (ROS)-generating activity of blood plasma polymorphonuclear leucocytes and ascitic fluid macrophages was studied during tumor growth in animal organisms. It was found that, in the initial period of tumor growth, 8 × 10 −5 M sodium nitroprusside (SNP), which is an NO donor, reduced the potential ROS-generating activity of macrophages by 38.5 ± 9% and plasma polymorphicnuclear leucocytes by 27.6 ± 7%. However, the dynamics of this process during the tumor growth was conservative and variations in ROS production by phagocytes were 10 ± 3%. L-arginine induced a decrease in the ROS-generating activity of granulocytes and mononucleares by 25–30%. The results point to inducible inhibition effect of NO-synthase on the ROS-generating activity of NADPH-oxidase in the course of tumor growth. Nitroarginine, an inhibitor of NO-synthase, produced stable increase in the ROS-generating activity of phagocytes isolated from the tumor at different periods of its growth. The use NO-synthase inhibitors to increase the ROS level in the area of tumor growth may favor the suppression of tumor-cell growth in vivo.

The influence of weak magnetic fields of different types on the rate of the formation of reactive oxygen species in mouse peritoneal neutrophils has been studied. It was found that the exposure of neutrophils activated by phorbol 12-myristate 13-acetate to the magnetic field tuned to the parametric resonance for Ca2+ ions leads to a decrease in the rate of the reactive oxygen species (ROS) generation by 23%. Conversely, the generation of ROS in neutrophils exposed to the same field but stimulated by the bacterial peptide FMLP (N-formyl-L-methionyl-L-leucyl-L-phenylalanine) increased by about 21%. Pulsed magnetic fields also changed the rate of ROS generation in phorbol-stimulated neutrophils by about 20%, but the sign of the effects observed in this case was opposite to those induced by the magnetic field tuned to the parametric resonance for Ca2+ ions.

Dihydroquercetin (flavonoid of plant origin) immobilized with an amino acid in lecithin nanoparticles promotes reduction of inflammatory reactions in the wound after thermal burn. The use of a liposomal complex in burn injury stabilizes endogenous antioxidant system and limits the secondary necrotic zone in the wounds. The treatment was associated with intensification of skin regeneration processes and reparation of hairy follicles and sebaceous glands.

It was found that dihydroquercetin, a flavonoid of plant origin, localized in lecitin nanoparticles with glycine amino acid, reduced inflammatory reactions in wound zones after thermal burns. The application of the liposomal complex to burn trauma stabilized the endogenous antioxidant system and minimized the area of secondary necrosis in the wound. The intensification of skin regeneration and repair of hair follicles and sebaceous glands were also observed.

Liposomes containing natural flavonoid dihydroquercetin, phospholipid lecithin, and zwitterionic amino acid glycine were used for the therapy of glacial acetic acid-induced chemical burn. No inflammatory reaction was observed in the region of wound. The area of postburn injury did not increase in time. Planimetry and histological studies showed that improved skin regeneration was accompanied by repair of hair follicles and sebaceous glands.

The effects of pyrimidine derivative 3,4-dihydro-2(1H)-pyrimidinethione, (DPT) used as a test-system for detection of tumor growth, on the goldfish Mauthner neurons (MN) ultrastructure and function, as manifested in behavioral changes, were studied. The results of investigations demonstrated that an application of DPT on MN had the effects similar to those of dopamine application, as established earlier, causing the enhancement of MN resistance to fatigue stimulation, accompanied by an increase of the dimensions of the actin containing desmosome-like afferent admembranous synaptic contacts, and formation of the cytoplasmic bundles of actin stress-fibers. Similarity of morpho-functional changes of MN, induced by DPT, an artificial chemical substance, which has no receptors on the neuronal membrane, and by natural neurotransmitter dopamine, allows us to suggest possible trophic stabilizing and polymerizing effects of both substances on cytoskeletal actin due to their direct penetration into postsynaptic neuron.

Amyloid oligomers, protofibrils, and fibrils of various amyloidogenic proteins are known to induce cell death. Tetracycline prevents the formation of fibrils of Aβ peptide and other amyloidogenic proteins and decomposes mature fibrils. It was previously shown that sarcomeric cytoskeletal proteins of the titin family (protein X, protein C, and protein H) in vitro form amyloid fibrils and tetracycline decomposes them. In this work, the concentration and time dependence of the survival of polymorphonuclear leukocytes in the presence of protein X amyloid fibrils is demonstrated. It is also shown that the survival rate increases as fibrils are decomposed by tetracycline. The antibiotic itself is found to be nontoxic. The results obtained show that this approach can be used to evaluate the efficiency of drugs that prevent or rectify amyloidoses.

The generation of reactive oxygen species (ROS) by polymorphonuclear leukocytes (PMNL) and the role of Ca(2+) in regulating their activity during Zajdela hepatoma growth in the animal peritoneal cavity were studied. We found a marked increase in the ROS-generating activity of PMNL in circulating blood, the result of increases in both the specific activity of leukocytes and total number of PMNL in circulating blood. The ROS-generating activity of PMNL was substantially activated by Ca(2+) ions and a calcium ionophore (ionomycin), but this effect virtually completely disappeared during tumor growth. Perhaps the high ROS-generating activity of PMNL and the lack of the sensitivity to extracellular Ca(2+) during tumor growth in the organism are due to an accumulation of intracellular Ca(2+) ions.