In this work, oxidative damage and the level of antioxidant response in Acinetobacter calcoaceticus, Pseudomonas putida, and Rhodococcus erythropolis cells under the influence of such antibiotics as ampicillin, azithromycin, rifampicin, tetracycline, and ceftriaxone were studied. The level of protein carboxylation and lipid peroxidation (LPO), as well as the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), and the level of glutathione 3 and 6 hours after antibiotic treatment of bacteria were assessed. It is observed that SOD induction occurs earlier and is more active than catalase induction. In A. calcoaceticus, SOD is induced together with protein carboxylation and probably protects them from oxidative damage, while catalase induction correlates with LPO. A positive correlation is also noted between catalase activity and glutathione content in R. erythropolis. Catalase activity increases insignificantly and even decreases under the studied antibiotics influence, which is associated with an insignificant level of lipid peroxidation in most prokaryotes. On the other hand, low catalase activity can contribute to genome destabilization as a result of oxidative stress and enhance the adaptive evolution of bacteria.

In this work, oxidative damage and the level of antioxidant response in Acinetobacter calcoaceticus, Pseudomonas putida, and Rhodococcus erythropolis cells under the influence of such antibiotics as ampicillin, azithromycin, rifampicin, tetracycline, and ceftriaxone were studied. The level of protein carboxylation and lipid peroxidation (LPO), as well as the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), and the level of glutathione 3 and 6 hours after antibiotic treatment of bacteria were assessed. It is observed that SOD induction occurs earlier and is more active than catalase induction. In A. calcoaceticus, SOD is induced together with protein carboxylation and probably protects them from oxidative damage, while catalase induction correlates with LPO. A positive correlation is also noted between catalase activity and glutathione content in R. erythropolis. Catalase activity increases insignificantly and even decreases under the studied antibiotics influence, which is associated with an insignificant level of lipid peroxidation in most prokaryotes. On the other hand, low catalase activity can contribute to genome destabilization as a result of oxidative stress and enhance the adaptive evolution of bacteria.

Soil pollution with heavy metals not only reduces crop yields, but also negatively affects human and animal health. Even such a biophilic element as Zn, when excessively supplied to living organisms, has a toxic effect. The introduction of sorbents into the soil makes it possible to ensure the binding of pollutants in situ, leading to a decrease in their mobility and biological availability. In the course of the work, the efficiency of application and the physicochemical characteristics of organic carbonaceous sorbents, granular activated carbon (GAC) of commercial production and biochar obtained from regional agricultural waste (rice husk) were investigated and compared, which determine their adsorption capacity with respect to Zn ions. Under the conditions of a model experiment, metal inactivation was shown in contaminated soils when using carbonaceous sorbents. Due to the high sorption properties of GAC and biochar, a decrease in the content of all mobile forms (exchange, complex and specifically sorbed) of Zn compounds in contaminated soils, was found. The most effective dose for reducing the mobility of metal ions in the soil was 5% of the soil mass for both biochar and GAC.

Objectives. To study the relationship between measures of oxidative stress and clinical changes in patients with neurodegenerative parkinsonism and identify clinical and biological subtypes of the disease. Materials and methods. The study included 109 subjects, of whom 91 were patients with neurodegenerative parkinsonism (72 patients with Parkinson’s disease (PD), 10 with multisystem atrophy (MSA), nine with corticobasal degeneration; mean age 61.1 ± 7.2 years) and 18 were clinically healthy people, mean age 55.1 ± 9.2 years. Peripheral blood redox status in PD patients and healthy subjects was assessed by assay of indicators of oxidative stress. Biochemical indicators were determined in RBC and mononuclear blood cells. Glutathione reductase (GR) and myeloperoxidase (MPO) activities were assayed, along with reduced glutathione levels. Results and conclusions. Oxidative stress is a universal mechanism and is seen in many neurodegenerative diseases. Nonetheless, quite characteristic changes in redox balance could be detected, defining groups and correlating them with particular subtypes and courses of PD, providing an opportunity for differential diagnosis from atypical parkinsonism.

To study the role of paraoxonase, myeloperoxidase, arginase, asymmetric dimethylarginine, and nitric oxide in the mechanisms of the pathogenesis of postpericardiotomy syndrome (PPCS), 76 patients with ischemic heart disease (IHD) who underwent coronary artery bypass grafting were examined. Patients were divided into two groups: Group 1, IHD patients who were not diagnosed with PPCS as a result of clinical studies, and Group 2, IHD patients who were diagnosed with PPCS. The results indicate that the postoperative period after coronary artery bypass grafting is associated with the inhibition of paraoxonase, the activation of myeloperoxidase, enhanced arginase activity, increased nitrite/nitrate and asymmetric dimethylarginine levels; it may also be accompanied by the development of endothelial dysfunction and increased systemic inflammatory response. In the present work, inverse correlations were found between the paraoxonase aryl esterase activity and myeloperoxidase activity in plasma, as well as the paraoxonase aryl esterase activity in blood plasma and arginase activity in erythrocytes in patients of both groups. Tests to predict the development of postpericardiotomy syndrome were developed based on the ratio of activity of the studied enzymes.

Here, we studied the effect of the mitochondria-targeted antioxidant SkQ1 (plastoquinone cationic derivative) on the CASP3 gene expression and caspase-3 activity in rat cerebral cortex and brain mitochondria under normal conditions and in oxidative stress induced by hyperbaric oxygenation (HBO). Under physiological conditions, SkQ1 administration (50 nmol/kg, 5 days) did not affect the CASP3 gene expression and caspase-3-like activity in the cortical cells, as well as caspase-3-like activity in brain mitochondria, but caused a moderate decrease in the content of primary products of lipid peroxidation (LPO) and an increase in the reduced glutathione (GSH) level. HBO-induced oxidative stress (0.5 MPa, 90 min) was accompanied by significant upregulation of CASP3 mRNA and caspase-3-like activity in the cerebral cortex, activation of the mitochondrial enzyme with simultaneous decrease in the GSH content, increase in the glutathione reductase activity, and stimulation of LPO. Administration of SkQ1 before the HBO session maintained the basal levels of the CASP3 gene expression and enzyme activity in the cerebral cortex cells and led to the normalization of caspase-3-like activity and redox parameters in brain mitochondria. We hypothesize that SkQ1 protects brain cells from the HBO-induced oxidative stress due to its antioxidant activity and stimulation of antiapoptotic mechanisms.

The administration of SkQ1 to rats at the dose of 50 nmol/kg for five days significantly increased the mRNA levels of transcription factor Nrf2 and of Nrf2-controlled genes encoding antioxidant enzymes SOD1, SOD2, CAT, and GPx4, whereas changes in the level of mRNA of SOD3 in the cerebral cortex of the rat brain were not significant. This was accompanied by activation of antioxidant enzymes (SOD, CAT, GPx, and GST) and increase in reduced glutathione concentration. Under oxidative stress induced by hyperoxia (0.5 MPa for 90 min), the mRNA level of transcription factor Nrf2 decreased, whereas changes in the transcriptional activity of Nrf2-induced genes (SOD1-3, CAT, GPx4) encoding antioxidant enzymes in the cortex of the rat brain hemispheres were insignificant. Under conditions of hyperoxia, lipid peroxidation intensity was increased, CAT was inhibited, and GST activity was moderately increased, whereas SOD and GPx activities in the rat brain cerebral cortex remained at the stationary level. Pretreatment with SkQ1 before the exposure to hyperbaric oxygenation led to an increase in mRNA level of transcription factor Nrf2 and of Nrf2-induced genes (SOD1-2, CAT, and GPx4) encoding antioxidant enzymes, whereas SOD3 expression in the cerebral cortex of the rat brain under oxidative stress was not changed. Concurrently, we observed an increase in activities of these antioxidant enzymes (SOD, CAT, GPx, and GST) and in level of reduced glutathione. We hypothesize that the protective effect of SkQ1 under hyperoxia-induced oxidative stress could be realized via direct antioxidant activity and through stimulation of the signaling defense system Keap1/Nrf2/ARE.

Traumas are among the leading risk factors for the development of osteoarthritis of the knee (OA). The aim of the present work was to study the associations between polymorphisms in the nNOS and eNOS genes and the risk of the development of post-traumatic osteoarthritis of the knee (PTOA) among residents of Rostov region. The results indicate the development of nitrosative stress in blood plasma and synovial fluid (SF) in PTOA. However, the nitrite/nitrate content in the SF was associated with the genotype of the‒786T > C locus of the eNOS gene; carrying the–786 С mutant allele leads to a decrease in the NOx − content. The –84A allele of the polymorphic nNOS gene can be associated with the risk of the development of PTOA and intensification of chondrocyte apoptosis, which is confirmed by the electron-microscopic study of cartilage tissue containing early and late apoptotic chondrocytes.

The identification of biomarkers of post-traumatic osteoarthritis (PTOA) progression is of clinical importance. The aims of this study were: (1) to assess the abilities of various soluble proinflammatory mediators in plasma to distinguish patients with knee PTOA from controls; (2) to determine the correlations between the mediators in plasma and those mediators in synovial fluid (SF); and (3) to explore the associations of the mediators with radiographic PTOA severity.

The study demonstrated that oxidative stress induced by hyperoxia (0.5 MPa for 90 min) resulted in reduction of mRNA levels of transcription factor Nrf2 and Nrf2-induced genes encoding antioxidant enzymes (SOD1, CAT, GPx4) in peripheral blood leukocytes of rats. The changes in gene expression profiles under hyperoxia were accompanied by disbalance of activity of antioxidant enzymes in the leukocytes, namely activation of superoxide dismutase and inhibition of catalase, glutathione peroxidase, and glutathione-S-transferase. Pretreatment of rats with SkQ1 (50 nmol/kg for five days) significantly increased mRNA levels of transcription factor Nrf2 and Nrf2-induced genes encoding antioxidant enzymes SOD2 and GPx4 and normalized the transcriptional activity of the SOD1 and CAT genes in the leukocytes in hyperoxia-induced oxidative stress. At the same time, the activity of catalase and glutathione peroxidase was increased, and the activity of superoxide dismutase and glutathione-S-transferase returned to the control level. It is hypothesized that protective effect of SkQ1 in hyperoxia-induced oxidative stress can be realized via a direct antioxidant property and the stimulation of the Keap1/Nrf2 redox-sensitive signaling system.

Specific features of the regulation of free-radical oxidation in the blood and synovial fluid in knee osteoarthritis were studied. We examined 46 individuals with an average age of 63.26 ± 9.18 years with primary knee osteoarthritis at stages II–III and 27 almost healthy individuals. The enhanced superoxide eliminating activity of the blood plasma was accompanied by a tendency of an increase in nitrosative stress markers, the nitrites/nitrates. In the erythrocytes we observed an increased level of the secondary product of lipid peroxidation, malone dialdehyde, as well as the activation of the superoxide dismutase and glutathione S-transferase with decreased activity of the glutathione peroxidase and a reduced glutathione content. In knee osteoarthritis, the mononuclear cells of the peripheral blood were characterized by considerable activation of the superoxide dismutase and glutathione S-transferase, moderate activation of the catalase, and slight changes in the glutathione peroxidase activity, together with the enhanced activity of the xanthine oxidoreductase and myeloperoxidase. The redox balance disturbance in the mononuclear cells led, in the long run, to oxidative stress development, which contributed to an increased level of lymphocyte apoptosis.

The data concerning the balance of pro-oxidants and antioxidants in the blood cells (lymphocytes) and synovial fluid in patients with osteoarthritis of the knee are considered and analyzed. Besides, known markers of oxidative and nitrosative stress and the intensity of lymphocytes’ apoptosis bound with this joint disorder are discussed; the obtained results can be applied as tests in diagnosis and medical treatment.

Purpose: The aim of the present study to investigate the role of glutathione-dependent enzymes in the regulation of blood and synovial fluid redox-balance in patients with osteoarthritis of the knee joint.Materials and methods: In the blood and synovial fluid of the three groups of patients with osteoarthritis of the knee joint, undergoing various treatment, the glutathione-dependent enzymes activity was determined.Results: A significant changes in glutathione-dependent enzymes activity in osteoarthritis, characterized by decreased level of glutathione and a significant inhibition of glutathione peroxidase and glutathione-S-transferase in synovial fluid and disturbance of glutathione-dependent system function in blood has been shown.Summary: Increased oxidative stress in osteoarthritis have led to compensatory changes in the glutathione level and antioxidant enzymes activity in blood. These findings confirm that glutathione-dependent system components can serve as markers for disease activityand effectiveness of treatment

В статье приведены и проанализированы данные о состоянии баланса прооксиданты-антиоксиданты в клетках крови (лимфоциты), а также синовиальной жидкости пациентов с диагнозом гонартроз. Кроме того, рассмотрены известные маркеры оксидативного и нитрозильного стресса и интенсивность апоптоза лимфоцитов периферической крови при данной суставной патологии, что может служить прогностическим тестом в диагностике и терапии.