The hydroperoxyl radical (•OOH), a reactive oxygen species (ROS), plays a critical role in regulating physiological processes. Its involvement in cellular redox pathways and association with pathological processes make it a key molecule for understanding how excessive free radicals modulate cellular metabolism. This study investigated the effects of exogenous •OOH on the redox metabolism of mononuclear cells during phagocytosis. Rat-derived mononuclear cells were treated with different concentrations of •OOH (generated via spark-discharge non-coherent radiation), and phagocytosis was induced using latex particles. The effect of •OOH on cell membrane integrity was assessed by trypan-blue-staining, while redox metabolites were quantified by spectrofluorimetry and spectrophotometry at 1-, 30-, and 60-minutes post-phagocytosis induction. In unexposed cells, free FAD and NADH levels increased during phagocytosis, tryptophan-containing proteins remained stable, and glycation end-products (AGEs) rose significantly by 60 minutes post-phagocytosis induction. •OOH at concentrations of (3.6 ± 0.9) × 10⁻⁵ and (1.8 ± 0.45) × 10⁻⁴ mol/L did not alter redox metabolism. However, exposure to higher concentrations ((5.4 ± 1.35) × 10⁻⁴ mol/L) induced significant cytotoxic effects. At the metabolic level, this dose triggered a marked redox imbalance, evidenced by a 1.4-fold increase in FAD, altered coenzyme ratios (NADH/FAD and NADH/NAD), and a significant decrease in tryptophan-related protein fluorescence, indicating extensive macromolecular damage. All •OOH concentrations tested suppressed the formation of AGEs 60 minutes after phagocytosis induction. We propose that this inhibition is not due to a protective effect, but to fragmentation of the protein backbone or modifications in the side chains induced by radicals.
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 02_14-29.pdf | 1.16 MB |
Background: Children with Autism Spectrum Disorder (ASD) often struggle with movement coordination and social interaction. Yoga practices have shown potential in easing behavioural and sensory issues, but their long-term effects on motor skills and autism symptoms remain unclear. This study explored whether extended yoga sessions could improve neuromuscular function (NMF) and autism severity (AS) in children with ASD. Methods: Sixty children aged 5–15 years with ASD were randomly assigned to a Yoga Group (YG, n = 30) or Control Group (CG, n = 30). The YG participated in structured yoga sessions for 60 minutes daily, five days a week, over a six-month period. NMF was assessed using auditory reaction time (ART), visual reaction time (VRT), and postural stability (PS). AS was evaluated using the Childhood Autism Rating Scale (CARS) and Autism Diagnostic Observation Schedule (ADOS). Assessments were carried out at baseline then 3 months, and 6 months. Results: By six months, the YG showed significant improvement in ART (450 ± 10 m.s.), VRT (500 ± 12 m.s.), and PS (1.6 ± 0.5) compared to the CG (p < 0.001). The CARS score in YG reduced to 28.9 ± 4.5 versus 35.7 ± 5.3 in CG. ADOS communication and social interaction scores also improved significantly in YG (p < 0.001). Conclusion: Long-term yoga sessions enhanced motor responses and reduced autism-related symptoms, indicating potential as a supportive therapy for ASD.
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| 01_5-13.pdf | 685.51 KB |
The aim of the study was to evaluate the impact of regular physical activity on the gut microbiota architecture and associated metabolic modules in 8- to 10-year-old children. Participants were divided into two groups: controls (Group 1) and those who had been practicing taekwondo for over two years outside of school physical education (Group 2). The metagenomic component was based on sequencing of the 16S rRNA V1–V9 regions; the data were analyzed within a pipeline using Minimap2, Emu, and network analysis in R (vegan, igraph, ggraph). The results indicate that Group 2 exhibits a more complex microbiota network, highlighting specific modules associated with fiber processing and the synthesis of anti-inflammatory SCFAs, including butyrate and propionate. A direct link between metabolic pathways and immune regulation was observed through effects on regulatory T cells, IgA, and anti-inflammatory signaling. Network module analysis identified a core anti-inflammatory microbiota in athletes (modules 1, 4, 6, 8, 9, 13, 25) and found enhanced lactate and succinate detoxification mechanisms. These findings highlight the role of physical activity in restructuring the functional architecture of the microbiota and increasing intestinal resistance.
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| 17_Шепилова_180-213.pdf | 3.4 MB |
This paper summarizes five years of monitoring opportunistic bacteria in laboratory primates and assessing their phage sensitivity. The main representative of the microbiota in both healthy and sick animals was lactose-positive Escherichia coli (84.6% and 92.7%, respectively). Among other enterobacteria, Proteus spp., Enterobacter spp., and Klebsiella spp. were most frequently detected. Molecular genetic analysis revealed widespread circulation of pathogenic groups of E. coli, primarily enteroinvasive (92.9%) and enteropathogenic (63.4%) strains. Staphylococcus aureus carriage was noted in 41.6% of animals. Assessment of the lytic activity of bacteriophages showed limited effectiveness of phages targeting Gram-negative enterobacteria: Intesti bacteriophage lysed 25% of cultures, Klebsiella bacteriophage lysed 3.4%, and Proteus phages lysed 22.2-55.5%. In contrast, staphylococcal bacteriophage CH1 was active against all S. aureus cultures. No bacteriophages with broad activity against EIEC, EPEC, Klebsiella spp. or Proteus spp. were identified. The data highlight the similarity between primate and human microbiota and the need for individualized selection of bacteriophages to ensure microbiological safety and increase the effectiveness of phage prophylaxis in laboratory animal husbandry.
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| 16_Черкашина_171-179.pdf | 811.35 KB |
Noroviruses are the leading cause of outbreaks of nonbacterial gastroenteritis and the second most common cause of all viral intestinal infections. An effective norovirus vaccine is expected to help reduce the incidence of intestinal infections, but intensive efforts to develop such a vaccine have so far been unsuccessful. Failures in vaccine development may be due to the high heterogeneity of noroviruses and/or the hypothetical low protective efficacy of the immune response to the most common virus variants, such as GII.4 Sydney 2012. The subject of the study was potential vaccine components – virus-like particles (VLPs), formed from VP1 of norovirus GII.4 Sydney 2012 (VP1N) and VLPs from a fragment of this protein containing the shell domain and hinge region (SN). We investigated the effect of VLPs on the ability of human dendritic cells (DCs) to recruit T cells into the immune response in vitro. VLP-treated DCs were cultured with pure CD4+ T cells, and then T cell maturity and cytokine production were assessed. It has been shown that VP1N-treated DCs, but not SN-treated DCs, have an increased ability to shift the ratio of T cell from naïve T cells to more mature central memory T cells and stimulate IL-17 production. Intracellular cytokine assay revealed no differences in T-helper type 1 (Th1), Th17 and Th1/17 levels between mixed cultures with VP1N-treated DCs and control DCs. Apparently, the increase in IL-17 production occurs due to an increase in the activity of mature Th17, and not the maturation of new producer cells.
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| 15_Талаев_162-170.pdf | 684.84 KB |
Radiation therapy is a fundamental part of the treatment of many oncological diseases. It is used both as a primary treatment modality and adjunct to other treatment approaches, with therapeutic intent ranging from curative to palliative interventions. Different dose rates exert differential biological effects in the cells - a phenomenon known as the dose-rate effect. For example, the severity of DNA damage, cell cycle progression and cellular senescence was strongly influenced by the dose rate of corpuscular radiation. Valuable insights into the mechanisms underlying tumor cell responses to ionizing radiation can be gained by analyzing changes in the expression of genes involved in radiation-induced cellular reactions using standardized real-time quantitative polymerase chain reaction (qPCR). However, accurate interpretation of qPCR data is often complicated by challenges in selecting appropriate reference genes for normalization. The effects of ionizing irradiation in this case introduce more unpredictable, due to variability in both the extent and the nature of damage. These variations can result in delays or even arrest of the cell cycle, subsequently leading to pronounced alterations in the expression profiles of numerous cellular proteins, including the housekeeping genes. This study aimed to determine the reliable reference genes for assessment of gene expression changes in tumor cells exposed to high-dose rate and low-dose rate irradiation. We found differences in the stability of expression of traditionally used housekeeping genes depending on the irradiation dose rate.
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| 14_Сороко_152-161.pdf | 551.66 KB |
Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. Heart failure (HF), a major pathology of the myocardium, is characterized by impaired cardiac function that leads to an abnormal enlargement of the heart, known as hypertrophy. In the study of the molecular mechanisms of HF pathogenesis, animal models play a crucial role. To characterize induced HF in animal models, biochemical approaches, such as quantifying the concentration of biomarkers in blood serum, are extremely important. Here we report a new immunochemical test system based on the measurement of the concentration of the B-type natriuretic peptide, protein biomarker of HF and hypertrophy, that can be utilized for characterization of HF development in rats and serve as a tool for further BNP concentration analysis.
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| 13_Серебряная_145-151.pdf | 497.15 KB |
Oncopathology, along with cardiovascular diseases, are the leading causes of premature death in most countries worldwide. Approximately 90% of all malignant tumors are multifactorial diseases that develop in the presence of a hereditary predisposition under the influence of both modifiable and non-modifiable factors. Non-modifiable factors include gender and age. Modifiable factors include stress, hormonal imbalances, environmental pollution, and dietary habits. The risk of cancer development and progression is increased by the consumption of meat, processed meat products, and sausages containing carcinogenic nitroso compounds, into which vegetable nitrates are also converted. Excess table salt, polycyclic aromatic hydrocarbons, benzopyrene, trans fats and acrylamide also contribute to oncopathology. Antitumor properties are possessed by dietary fiber, isoflavones, Bowman-Birk inhibitors, lectins, omega-3 and omega-6, flavonoids, carotenoids, sesamin, spermidine, chlorophyll, and epigallocatechin contained in raw and processed plant products without frying. This article describes the mechanisms of action of these food components, the study of which can form the basis for comprehensive cancer treatment and the development of new methods of antitumor therapy.
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| 12_Мустафин_129-144.pdf | 349.22 KB |
Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder in which neuroinflammation plays a major role in its pathogenesis, alongside the formation of amyloid plaques and neurofibrillary tangles. Necroptosis, a recently discovered regulated form of cell death mediated by the kinases RIPK1 and RIPK3, is considered one of the mechanisms contributing to neuroinflammation and neuronal death in AD. In this study, we evaluated the effect of chronic necroptosis inhibition using Necrostatin-1, a RIPK1 blocker, on the progression of neurodegeneration in aged 5xFAD mice, a model of the familial form of AD. Over a 12-week treatment period, the animals’ neurological status was assessed, followed by evaluation of long-term memory using the Morris water maze test, histological analysis of the prefrontal cortex and hippocampus, and RT-PCR analysis of the expression of key genes associated with necroptosis and inflammation. Chronic administration of Nec-1 significantly slowed the progression of neurological deficits in both male and female 5xFAD mice. Inhibition of necroptosis prevented the loss of normal neurons, reduced the number of hyperchromic cells, and decreased the severity of pericellular and perivascular edema in the examined brain regions. However, in the Morris water maze test, learning and memory improved only partially in males, but not in female 5xFAD mice. This may be attributed to the increased expression of the anti-inflammatory cytokine IL-10 in the cortex and hippocampus of males. The results obtained indicate that inhibition of necroptosis by Necrostatin-1 represents a promising therapeutic approach for correcting neurological impairments and mitigating morphological brain alterations in Alzheimer’s disease.
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| 11_Митрошина_113-128.pdf | 1.74 MB |
Objective: To investigate the levels of exhaled nitric oxide (FeNO) in children with mild bronchial asthma (BA) depending on disease control and the dynamics of FeNO levels after a 3-month course of treatment with leukotriene receptor antagonists (LTRA) or low doses of inhaled glucocorticosteroids (ICS). Materials and Methods: One hundred twenty children aged 5-15 years were examined, including 90 children with mild BA and 30 healthy controls. Measurements included FeNO, concentrations of nitrite (NO2-), nitrate (NO3-), their total concentration (TNN), and 3-nitrotyrosine in exhaled breath condensate. The main group was randomized into two subgroups: subgroup A - 60 children receiving montelukast, and subgroup B - 30 children receiving ICS. Results: In children with partially controlled BA, levels of FeNO, TNN, and NO3- in exhaled breath condensate were significantly higher compared to those with fully controlled BA. Following treatment with LTRA and ICS, a significant reduction in FeNO, TNN, and NO3- was observed in both subgroups. Conclusion: Dysregulation in the nitric oxide system plays a significant role in the pathogenesis of BA in children. Measurement of nitric oxide cycle parameters may be utilized for monitoring the effectiveness of basic therapy.
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| 10_Кубышева_105-112.pdf | 558.49 KB |
