Activation Of Peroxidation Research Articles

Bach2 repression of CD36 regulates lipid-metabolism-linked effector functions in follicular B cells

The transcription repressor Bach2 plays a crucial role in shaping humoral immunity, but its cell-autonomous function remains elusive. Here, we reveal the mechanism by which Bach2 regulates effector cell maturation in peripheral B cells. In response to Toll-like receptor (TLR) agonists, Bach2 deficiency promotes the differentiation of follicular, but not marginal zone, B cells into effector cells, producing interleukin (IL)-6 and antibodies. This phenomenon is associated with changes in lipid metabolism, such as increases in CD36 expression, lipid influx, and fatty acid oxidation. Consistent with this, Bach2-deficient B cells exhibit elevated levels of mitochondrial oxidative stress, lipid peroxidation, and p38 activation. Mechanistically, Bach2 acts as a repressor of Cd36, and inhibition of CD36 or fatty acid oxidation reduces the differentiation of naive B cells into IL-6- and antibody-secreting cells. These results indicate Bach2 as a key metabolic checkpoint regulator crucial for maintaining a functionally quiescent state of follicular B cells.

Dynamics of Free Radical Oxidative Processes During the Latent Period of Experimental Metastasizing to the Liver

Purpose — to investigate the dynamics of the content of antioxidant enzymes superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPO1), glutathione reductase (GR) and lipid peroxidation products diene conjugates (DC), malondialdehyde (MDA) in the spleen and liver during the latent period of growth and metastasis of experimental tumor.Materials and methods. Using 28 white male rats, a model of hematogenous liver metastasis was created by transplanting sarcoma 45 cells (S45) into the spleen, previously lead out under the skin 3 weeks before. Previously, was determined that a tumor visualized in the spleen at 5 weeks, and liver metastases at 7 weeks after transplantation S45. Levels of SOD1, GPO1, GR and MDA were determined using ELISA and DC by biochemical method in spleen and liver homogenates during the latent period of tumor growth and metastasis (1–2 weeks post-transplantation).Results. Significant changes (1.5–5.2 times, р < 0.050–0.001) in studied factors levels were observed compared to intact rats and rats with the spleen lead out. Activation of lipid peroxidation and antioxidant system was noted in the spleen (tumor-carrying organ) during tumor growth and metastasis. At the same time, in the liver (the target organ of metastasis) observed also increased lipid peroxidation but simultaneously a pronounced decreased GR levels (5 times, p < 0.001) without affecting SOD1 levels.Conclusion. Liver tissue exhibited the inferiority of antioxidant protection and the formation of pro-oxidant condition during the latent period of tumor growth, which may prepare the soil for metastasis.

LRRK2 regulates production of reactive oxygen species in cell and animal models of Parkinson's disease.

Oxidative stress has long been implicated in Parkinson's disease (PD) pathogenesis, although the sources and regulation of reactive oxygen species (ROS) production are poorly defined. Pathogenic mutations in the gene encoding leucine-rich repeat kinase 2 (LRRK2) are associated with increased kinase activity and a greater risk of PD. The substrates and downstream consequences of elevated LRRK2 kinase activity are still being elucidated, but overexpression of mutant LRRK2 has been associated with oxidative stress, and antioxidants reportedly mitigate LRRK2 toxicity. Here, using CRISPR-Cas9 gene-edited HEK293 cells, RAW264.7 macrophages, rat primary ventral midbrain cultures, and PD patient-derived lymphoblastoid cells, we found that elevated LRRK2 kinase activity was associated with increased ROS production and lipid peroxidation and that this was blocked by inhibitors of either LRRK2 kinase or NADPH oxidase 2 (NOX2). Oxidative stress induced by the pesticide rotenone was ameliorated by LRRK2 kinase inhibition and was absent in cells devoid of LRRK2. In a rat model of PD induced by rotenone, a LRRK2 kinase inhibitor prevented the lipid peroxidation and NOX2 activation normally seen in nigral dopaminergic neurons in this model. Mechanistically, LRRK2 kinase activity was shown to regulate phosphorylation of serine-345 in the p47phox subunit of NOX2. This, in turn, led to translocation of p47phox from the cytosol to the membrane-associated gp91phox (NOX2) subunit, activation of the NOX2 enzyme complex, and production of ROS. Thus, LRRK2 kinase activity may drive cellular ROS production in PD through the regulation of NOX2 activity.

Biomarker responses in fish caged in a rice field during a bifenthrin application

The use of pesticides in integrated rice-fish farming could have an impact on fish health. The present study aimed to evaluate, for the first time, the biological effects of the insecticide bifenthrin on fish (Piaractus mesopotamicus and Hoplosternum littorale) using a caging experiment. Fish were divided into two sites: control (C) and bifenthrin exposure (BF). Two cages (n = 8 fish/cage) per species were placed separately at each site. The BF application (Seizer ®) was carried out with a coastal sprayer according to the BF recommended dose for rice cultivation (0.1 L/ha). After 72 hours, fish were collected, and gills, liver, brain, and muscle were dissected for the analysis of biomarkers of accumulation, oxidative stress, and neurotoxicity. In P. mesopotamicus, the main changes were observed in the muscle, where BF accumulated and induced neurotoxicity (inhibition of cholinesterase activity) and oxidative stress (activation of antioxidant enzymes, decreased glutathione levels, increased lipid peroxidation). The gills and liver also showed changes in some markers of the antioxidant system. In H. littorale, BF exposure induced changes in oxidative stress biomarkers in liver (activation of antioxidant enzymes and lipid peroxidation) and gill tissues (alteration in antioxidant markers). These results show that the use of bifenthrin in rice fields poses a risk to fish farming under current pesticide management practices. Furthermore, its use could affect other species in these agroecosystems, highlighting the need for further studies to assess the ecological and productive consequences in a context of increasing pyrethroid use worldwide.

Heteronuclear coordination polymers with imidazole ligand: Synthesis, characterization and alcohol oxidation activities

Two new heteronuclear Cd(II)/Pd(II) coordination polymers, [Cd2(µ-im)2(Him)4Pd(µ-CN)4]n (1) and [Cd(Him)2Pd(µ-CN)4]n (2) (Him: imidazole), have been synthesized under different conditions and characterized using elemental analysis, thermal analysis, FT-IR and Raman spectroscopy, single-crystal and powder X-ray diffraction techniques.. In 1, the Cd(II) ions are bridged by imidazolate ligands to generate 1D chain structure. Neighbouring 1D chains were linked by [Pd(CN)4]2- ions to form 3D framework. In 2, the metal ions are bridged by cyanide ligands to generate 2D [Cd2Pd2(µ-CN)4]n network. Furthermore, catalytic peroxidative oxidation activity of catalysts 1 and 2 was examined on the oxidation of benzyl alcohol using tertiary-butyl hydroperoxide (t-BuOOH) as the oxygen source. The compound 1 exhibited over 90 % product conversion at 80 °C in 24-hour reaction time. In addition, the catalyst exhibited high selectivity towards benzaldehyde and no over-oxidation product (benzoic acid) was detected.

ATF3 as a response factor to regulate Cd-induced reproductive damage by activating the NRF2/HO-1 ferroptosis pathway

Cadmium (Cd) has garnered significant attention due to reproductive toxicity in inducing ferroptosis. However, the specific mechanisms underlying Cd-induced germ cell ferroptosis remain poorly understood. This study aimed to systematically explore the molecular mechanisms of germ cell ferroptosis by investigating differential changes in transcription factors and proteins in male mice treated orally with CdCl2 (0.5 g/L) reaching postnatal day 60, alongside Leydig cell (TM3) and Sertoli cell (TM4) lines. Results demonstrated that Cd exposure led to increased iron overload and oxidative stress in mouse testes, disrupted intracellular mitochondrial morphology characteristic of ferroptosis. RNA sequencing revealed significant upregulation of Atf3 and Hmox1 in Cd-exposed germ cells, along with increased expression of ATF3 and HO-1. Intervention in ferroptosis or HO-1 effectively rescued cells from Cd-induced mortality by breaking the detrimental cycle between lipid peroxidation and HO-1 activation. Further findings showed that NRF2 and HO-1 expression was notably elevated upon ATF3 overexpression in TM3 and TM4 cells, activating the Keap1-Nrf2 pathway and triggering ferroptosis in testes, whereas NRF2 and HO-1 expression levels were reversed when ATF3 was silenced. This study provides novel insights into ATF3-mediated NRF2/HO-1 signaling in Cd-induced mitochondrial ferroptosis in testes, shedding light on the mechanisms underlying Cd-induced ferroptosis and testicular injury.

Effect of tetrapeptides KK1 and KK5 on the immunological parameters of rat spleen during passive smoking

One of the trends in experimental and clinical immunology is the creation of new immunomodulators aimed at correcting various variants of the pathology of the immune system. Of interest are non-toxic, hormone-free and protease-resistant tetrapeptides, homologue of the of adrenocorticotropic hormone fragment (15- 18). There is little data in the literature on the effect of the above immunomodulators on the immunological parameters of the rat spleen on xenobiotic exposure models, which makes research relevant in this aspect. For the first time, the effect of tetrapeptides with laboratory ciphers KK1 and KK5 on the immunological parameters of the spleen of 36 female Wistar rats with passive smoking was evaluated. The experimental rats were fumigated with tobacco smoke for 8 hours daily for 20 days. Synthetic tetrapeptides were administered intranasally at a dose of 40 micrograms per kg/day, starting from the 10th day of the experiment. It was found that the studied tetrapeptides had a unidirectional positive effect on the immunological parameters of the spleen of experimental animals with passive tobacco smoking. This was expressed in a tendency to restore the pool of cells with CD3, CD4, CD8, CD20 markers to the level of the control group, as well as spontaneous and induced cytokine production by splenocytes. The shifts in the parameters of the spleen identified in this work may be based on a number of possible causes. Firstly, passive smoke causes a stress response in rats, which is confirmed by previous studies on a similar model, on an increase in the level of stress hormones in the blood serum of Wistar rats. Secondly, the literature data indicate the activation of lipid peroxidation during smoking. Thirdly, it is known that under the action of tobacco smoke toxicants, the lymphoid cell line suffers the most, since their polyhydrooxidized metabolites accumulate in the bone marrow and lymphoid organs, causing hypoplasia of the central and peripheral organs of immunity. A visible sign of this phenomenon is a decrease in the cellularity in the spleen, which is established in this work. Considering that active and passive smoking causes hypoxia and increases lipid peroxidation, the use of tetrapeptides KK1 and KK5 as agents that improve the body’s adaptation to hypoxia and increase resistance to stress damage is justified. Thus, the tetrapeptides KK1 and KK5 have a positive immunomodulatory effect, reducing the toxic stress effects of passive smoking.

Antioxidant and Cytoprotective Effects of Different Compounds on Cyclophosphamide-induced Nephrotoxicity

Abstract: Cyclophosphamide is a drug derived from nitrogenous mustards and is mainly indicated for the anti-neoplastic clinic. When it is metabolized in the liver, it produces acrolein, a cytotoxic metabolite capable of generating damage to the body. The oxidative, nitrative and nitrosative stress are responsible for mediating this side effect since the toxicity of the drug induces the production of reactive species of oxygen (ROS) and nitrogen (RNS). These radicals are unstable and react with other molecules that can result in cellular lesions such as lipid peroxidation, enzymatic inactivation, and excessive activation of pro-inflammatory genes, producing molecules such as malonaldehyde (MDA) and nitric oxide (NO), representing oxidative stress markers. One of the consequences of these mechanisms is nephrotoxicity. In contrast, some compounds have direct or indirect antioxidante action, which are the objects of this study: gallic acid, aminoguanidine, chrysin, hesperidine, naringin, morin-5'-sulfonic acid sodium salt and spirulina. All of them are responsible for the nephroprotective activity when administered during experiments in vitro or in vivo. Thus, this observational bibliographic research is characterized as qualitative descriptive and explanatory, since it focuses on analyzing the antioxidant properties of compounds with possible potentials to inhibit the nephrotoxicity induced by cyclophosphamide and describe the results, in addition to clarifying the biochemical activities involved in the process.

Zinc oxide nanoparticles cause hepatotoxicity in rare minnow (Gobiocypris rarus) via ROS-mediated oxidative stress and apoptosis activation and inhibition of lipid peroxidation

Zinc oxide nanoparticles (ZnO NPs) measuring 30 ± 10 nm in diameter are utilized in various applications, including batteries, plastics, ceramics, cosmetics, flame retardants, and food. However, their potential impact and risk on aquatic ecosystems remain unclear. This study examined the hepatotoxic effects of dietary ZnO NPs in rare minnow. Three hundred rare minnows were fed diets containing 0 mg/kg, 20 mg/kg and 60 mg/kg of ZnO NPs for 60 days, with hepatotoxicity assessments at 15-day intervals. The histological data showed that ZnO NPs severely damage liver tissues, causing cytoplasmic vacuolization and irregular or missing nuclei. The treatment groups showed a significant rise in the liver injury index (P < 0.05). Moreover, there was a notable increase in zinc accumulation in the ZnO NPs groups compared to the control group (P < 0.05). ZnO NPs also reduced body weight and hepato-somatic index (HSI) in rare minnows. The enzyme activity results showed elevated levels of reactive oxygen species (ROS), total cholesterol (T-CHO), triglyceride (TG), acetyl Coa carboxylase (ACC), and fatty acid synthase (FAS) in the ZnO NPs fed groups, while total antioxidant capacity (T-AOC) and malondialdehyde (MDA) decreased. Further investigation found that accumulation of ZnO NPs in the liver tissues up-regulated the levels of genes related to antioxidant (mn-sod, cat and nf-κb), pro-apoptotic (bax) and lipogenesis (gpat3, dgat1a and dgat1b), while down-regulating genes associated with lipid catabolism (cpt1 and tpi1). These findings suggest that dietary ZnO NPs cause hepatotoxicity by inducing oxidative stress through ROS, triggering apoptosis, and inhibiting lipid peroxidation. The results indicate that ZnO NPs may pose a significant threat to aquatic animals and ecosystems.

Exploiting UPO versatility to transform rutin in more soluble and bioactive products

The discovery of unspecific peroxygenases (UPOs) completely changed the paradigm of enzyme-based oxyfunctionalization reactions, as these enzymes can transform a wide variety of substrates with a relatively simple reaction mechanism. The fact that UPO can exert both peroxygenative and peroxidative activity in either aromatic or aliphatic carbons, represents a great potential in the production of high value-added products from natural antioxidants. In this work, the flavonoid rutin has been considered as possible substrate for UPO from Agrocybe aegerita, and its peroxygenation or its peroxidation and successive oligomerization have been studied. Different experiments were performed in order to reduce the range of process variables involved and gaining insight on the behavior of this enzyme, leading to a multivariable optimization of UPO-based rutin modification. While trying to preserve enzyme activity this optimization aimed for maximizing the production of more soluble antioxidants. Reusability of the enzyme was evaluated recovering UPO using an enzymatic membrane reactor, revealing challenges in enzyme stability due to inactivation during the filtration stages. The influence of the radical scavenger ascorbic acid on product formation was investigated, revealing its role in directing the reaction towards hydroxylated rutin derivatives, hence indicating a shift towards more soluble and bioactive products.

Accelerated Fe2+ regeneration for efficient electro-Fenton oxidation of refractory pollutants through pore structure engineering

Electro-Fenton (EF) is efficient in decontaminating refractory pollutants but high consumption of Fe2+ as a hydrogen peroxide (H2O2) activator increases its operation cost. Designing EF system with accelerated Fe2+/Fe3+ cycling is crucial for both hydroxyl radical generation and Fe2+ dosage reduction. Here, we employed pore structure tailoring engineering to optimize pore size of mesoporous hollow carbon spheres (MHCS), achieving an improved H2O2 electro-synthesis and Fe2+ regeneration. MHCS with 8 nm surface pores yielded 81.33 mmol gcatalyst−1h−1 H2O2 and realized 51.2 % Fe2+ regeneration efficiency, enabling complete removal of sulfamethazine with a low energy consumption of just 0.87 kWh g−1 total organic carbon. Finite element simulation revealed that MHCS with 8 nm surface pores favored mass transfer, facilitating solute diffusion to the electrode’s active layer for reaction. In addition, EF system maintained a degradation efficiency of 90 % after five cycles of operation and was effective in removing various types of pollutants, which implies its application potential. This work demonstrated a novel catalyst structure optimization strategy to both enhance Fe2+ regeneration and improve EF performance, offering an energy-efficient water purification solution.

Oxidative response to cadmium and lead accumulations in the tissues of blue swimming crabs Portunus pelagicus from the Trang Province coastline, Southern Thailand.

Metals have been reported to alter the oxidative status of both redox-active and redox-inactive metals accompanying oxidative stress induction. In aquatic ecosystems, metal contamination is regarded as serious pollutants and bioaccumulation, especially when aquatic seafood products are involved, which results in human risk. The blue swimming crab Portunus pelagicus is a highly popular crab species for consumption as seafood in Thailand. The meat parts and the hepatopancreas (HP) together with gonad are consumed and in high demand. Therefore, the present study aimed to investigate bioaccumulation of cadmium (Cd) and lead (Pb) along with tissue oxidative responses in P. pelagicus. Sixty-seven samples of P. pelagicus were obtained from small-scale fishers along the coastline of Trang Province. Bioaccumulation of Cd and Pb and oxidative response in gill, muscle, and HP + gonad were evaluated. Cadmium and Pb accumulation levels were highest in the HP and gonad, followed by the gill and then muscle, indicating that Cd and Pb have a high affinity to be concentrated in the HP and gonad. An organ-specific oxidative response to Cd and Pb accumulation was demonstrated in which Cd significantly activated superoxide dismutase (SOD) activity in the gills and muscle tissue, while Pb significantly activated the SOD activity only in the HP and gonad. Only Cd accumulation in gill tissue represented a significant activation of lipid peroxidation, as indicated by the malondialdehyde level. This study implied that P. pelagicus exhibits an "adaptive stage" in the oxidative response of tissue due to metal accumulation. Additionally, the data presented here further indicate that the consumption of only the meat parts and removal of the HP and gonad would reduce human exposure to metal toxicity.

A novel colorimetric sensor through peroxymonosulfate activated by CoFe@CN nanozymes for on-site resorcinol detection

The presence of resorcinol (RS) in water contaminated with pollutants may engender environmental and ecosystem risks. In this study, we developed rapid and efficient colorimetric methods for the on-site quantitative determination of RS. Specifically, a synthetic nanozyme composed of nitrogen-doped carbon-coated cobalt-iron (CoFe@CN) was utilized to initiate the oxidation reaction of 3,3′,5,5′-tetramethylbenzidine (TMB) with the activator of peroxymonosulfate (PMS). Compared to the activator of hydrogen peroxide (H2O2), PMS demonstrated a sixfold enhancement in catalytic efficacy, markedly elevating the detection performance. Density Functional Theory calculations indicate that RS can serve as a reducing agent for oxTMB, confirming the theoretical feasibility of this process. A linear relationship between inhibition rate (IR %) of RS concentration and absorbance was established and the colorimetric analysis revealed a linear relationship between RS concentration and gray scale values over the range of 0–45 μM, with a detection limit of 3.39 μM. Furthermore, smartphone-based analysis of color images allows for on-site quantitative analysis of RS concentration, leveraging portability and real-time detection capabilities. This study provides pioneering analytical support for on-site water quality monitoring within the ecological environment.

Biochemical and histological changes in two nonalcoholic fatty liver disease models of different severity

Background. One of the priority areas of modern medicine, which unites the interests of various specialists (therapists, cardiologists, gastroenterologists, endocrinologists), is the study of the pathogenesis and clinical manifestations of nonalcoholic fatty liver disease (NAFLD), which is widespread and of unconditional social significance. The search for adequate experimental models of NAFLD that reflect the severity of liver damage is of paramount importance for studying its etiology and pathogenesis.The aim of the study. To compare biochemical and histological changes in experimental models of NAFLD of varying severity.Materials and methods. Two NAFLD model versions were used: a light one – nonalcoholic steatosis (NAS) and a severe variant – non-alcoholic steatohepatitis (NASH). The following biochemical parameters were measured: enzyme activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (AP), plasma glucose concentration, total protein (TP), total bilirubin (TBil) and its conjugate fraction (CB), plasma concentrations of homocysteine (HC), total cholesterol (TC), triacylglycerides (TG), catalase (Cat), superoxide dismutase (SOD) and malondialdehyde (MDA).Results. When used in a model of steatohepatitis, liver function was impaired to a significantly greater extent than in the model of steatosis; this difference was manifested in a statistically significant increase in ALT, AST, AP, TC, Tbil, MDA (p &lt; 0.001) and a decrease in Cat, SOD (p &lt; 0.05). This is confirmed by the development of more pronounced symptoms of disorders of pigment and lipid metabolism, cytolytic and cholestatic syndromes, significant activation of lipid peroxidation and depression of the antioxidant system when modeling non-alcoholic steatohepatitis. Various degrees of severity of morphological changes in the experimental groups were revealed.Conclusion. The study showed the priority of determining biochemical markers, including the levels of ALT, AST, OBIL, TG, MDA and SOD to optimize laboratory methods for diagnosing the severity of liver dystrophy.The practical originality of the results lies in the optimization of the methodology for laboratory diagnosis of the severity of the pathological process in NAFLD.

Characterization of antimalarial activity of artemisinin-based hybrid drugs.

In response to the spread of artemisinin (ART) resistance, ART-based hybrid drugs were developed, and their activity profile was characterized against drug-sensitive and drug-resistant Plasmodium falciparum parasites. Two hybrids were found to display parasite growth reduction, stage-specificity, speed of activity, additivity of activity in drug combinations, and stability in hepatic microsomes of similar levels to those displayed by dihydroartemisinin (DHA). Conversely, the rate of chemical homolysis of the peroxide bonds is slower in hybrids than in DHA. From a mechanistic perspective, heme plays a central role in the chemical homolysis of peroxide, inhibiting heme detoxification and disrupting parasite heme redox homeostasis. The hybrid exhibiting slow homolysis of peroxide bonds was more potent in reducing the viability of ART-resistant parasites in a ring-stage survival assay than the hybrid exhibiting fast homolysis. However, both hybrids showed limited activity against ART-induced quiescent parasites in the quiescent-stage survival assay. Our findings are consistent with previous results showing that slow homolysis of peroxide-containing drugs may retain activity against proliferating ART-resistant parasites. However, our data suggest that this property does not overcome the limited activity of peroxides in killing non-proliferating parasites in a quiescent state.

ZIF-67/natural coal gangue composite as hydrogen peroxide activator for tetracycline hydrochloride degradation in water

The advanced oxidation process based on hydrogen peroxide (H2O2) can effectively degrade tetracycline hydrochloride (TC). The key to activating H2O2 for the degradation of organic pollutants lies in the exploration of efficient and cost-effective catalysts. Natural coal gangue (CG), a byproduct of coal mining, holds potential for use in catalytic oxidation of pollutants. Zeolitic imidazolate framework-67 (ZIF-67) is commonly employed to activate sulfate systems, serving as a highly efficient Co-based heterogeneous catalyst that promotes the generation of strong oxidation species. However, there has been no relevant research on using CG to load ZIF-67 for the activation of H2O2 in pollutant degradation. In this study, ZIF-67/CG catalysts were prepared, with ZIF-67 and CG serving as precursors for the highly efficient activation of H2O2. X-ray photoelectron spectroscopy (XPS) and Fourier-transform infrared spectroscopy (FTIR) confirmed that ZIF-67/CG possesses a favorable ability to activate H2O2. The results revealed that the degradation efficiency of TC in the ZIF-67/CG/H2O2 system reached 82.8% within 60 minutes. Radical quenching experiments, electron paramagnetic resonance (EPR) analysis, and an analysis of the degradation mechanism identified that ･OH and 1O2 played major roles in TC degradation.

ANALYSIS OF ANTIOXIDANT SYSTEM OF TEST ANIMALS IN THE DYNAMICS OF THE WOUND PROCESS AT LOCAL APPLICATION OF HYDROGEL DRESSINGS

Introduction. The development of the inflammatory process is always accompanied by the activation of lipid peroxidation, which is caused by tissue hypoxia. This, in turn, catalyzes a change in the physiological parameters of the antioxidant system. The aim of the study is to analyze the dynamics of the antioxidant balance of wounds in an experiment using hydrogels saturated with silver ions and an antioxidant drug for the local treatment of inflammatory processes. Object and research methods. The experimental study was carried out on 80 Wistar rats weighing 150 to 200 grams. Animals were removed from the experiment. for 3, 7, 10, 14 days. Catalase activity in the dynamics of the wound process was determined. Research results and their discussion. The content of catalase on the 7th day in the third experimental group is 0.51±0.03 μKat/l. On the 10th day, the indicator of the antioxidant system in the second (0.44±0.05 μKat/l) and third experimental groups was 0.42±0.02 μKat/l. At the final stage of the study on the 14th day, the analysis of catalase content showed that in all animals with a simulated inflammatory process, the indicator of antioxidant activity had no significant differences between themselves and, importantly, with the indicators of intact animals (0.33±0.01 μKat /l). The indicators of the control (0.33±0.04 μKat/l) and experimental groups were as follows: the first experimental group – 0.32±0.06, the second experimental group – 0.36±0.04, the third experimental group – 0, 38±0.06 μKat/l. Antioxidant protection was supplemented by local release of a drug with antioxidant action from the hydrogels, which contributed to a reduction in the intensity of free radical oxidation processes. That is, in almost all groups of animals, which were simulated purulent-inflammatory wounds, indicators of catalase activity approached the level of intact animals already on the 14th day. Conclusions. Application for local treatment of hydrogel bandages saturated with an antioxidant drug, which is released into the wound surface for a long time, promotes the activation of antioxidant protection and suppresses the processes of free radical formation.

Alcoholic cardiomyopathy: aspects of pathogenesis and clinic

Alcoholic cardiomyopathy is the most common form of myocardial damage caused by ethanol. Ethanol and its main active metabolite acetaldehyde have a direct toxic effect on the myocardium. The mechanisms of the cardiotoxic effect of ethanol are diverse and include membranotropic action, damage to cellular organelles, activation of lipid peroxidation, and a number of others. Dissolving in the lipids of biological membranes, ethanol changes their physico-chemical properties, disrupts the activity of membrane receptors, eventually disconnecting the connection of excitation with the contraction of cardiomyocytes. Particular importance in the pathogenesis of alcoholic cardiomyopathy is attached to the ability of ethanol to cause structural and functional changes in mitochondria, which is directly related to the violation of oxidative processes and energy supply of the myocardium as a whole. Under the influence of alcohol, free-radical lipid oxidation products content increases and antioxidants activity decreases, which indicates oxidative stress development. The deterioration of myocardial contractility due to chronic alcohol intoxication triggers a cascade of compensatory mechanisms in the form of cardiomyocyte hypertrophy and progressive fibrosis, while adaptive reactions become a factor in further pathological changes. Ethanol causes myocardial damage in a dose-dependent manner.The probability of alcoholic cardiomyopathy occurrence is a derivative of the total accumulated dose of alcohol and individual predisposition. Alcoholic cardiomyopathy is considered as a variant of secondary dilated cardiomyopathy with all its clinical manifestations and consequences: dilation of the heart chambers, low left ventricular ejection fraction, progressive circulatory insufficiency, and cardiac arrhythmias. A relatively favorable prognosis in alcoholic cardiomyopathy is provided due to partial reversibility of myocardial damage under the condition of abstinence from alcohol consumption. Specific drugs for the treatment of alcoholic cardiomyopathy have not been developed. New treatment strategies include the use of myocardial growth and regulation factors synthesized by cardiomyocytes, as well as the stimulation of heart muscle regeneration and repair processes.

Insight into the Discriminative Efficiencies and Mechanisms of Peroxy Activation via Fe/Cu Bimetallic Catalysts for Wastewater Purification.

Fe/Cu bimetallic catalysts have a synergistic effect that can effectively enhance catalytic activity, so Fe/Cu bimetallic catalysts have been extensively studied. However, the efficacy and mechanisms of Fe/Cu bimetallic catalysts' peroxidation activation have rarely been explored. In this study, Fe/Cu bimetallic materials were fabricated to catalyze different oxidizing agents, including peroxymonosulfate (PMS), peroxydisulfate (PDS), peroxyacetic acid (PAA), and hydrogen peroxide (H2O2), for the degradation of sulfamethoxazole (SMX). The Fe/Cu/oxidant systems exhibited an excellent degradation efficiency of sulfamethoxazole (SMX). In the Fe/Cu/PMS, Fe/Cu/PDS, and Fe/Cu/PAA systems, the main reactive oxygen species (ROS) responsible for SMX degradation were hydroxyl radical (•OH) and singlet oxygen (1O2), while the main ROS was only •OH in the H2O2 system. The differences in the surface structure of the materials before and after oxidation were examined, revealing the presence of a large amount of flocculent material on the surface of the oxidized PMS material. Anion experiments and actual body experiments also revealed that the PMS system had a strong anti-interference ability. Finally, a comprehensive comparison concluded that the PMS system was the optimal system among the four oxidation systems. Overall, this work revealed that the PMS oxidant has a better catalytic degradation of SMX compared to other oxidizers for Fe/Cu, that PMS generates more ROS, and that the PMS system has a stronger resistance to interference.

Пубертатний стрес спричиняє статевоспецифічні репродуктивні ефекти у дорослих щурів

Adolescence is one of the critical periods of individual development, which is highly sensitive to changes caused by stress factors. Stress-related hormonal imbalances can negatively affect puberty and reproductive function. The aim of the study was to investigate the long-lasting reproductive effects of chronic pubertal stress in rats. Animals were subjected to immobilization stress daily from 30 to 45 postnatal day by placing them for 1 h in cylinders 4.5 cm in diameter and 10 cm in long, equipped with breathing holes. The timing of puberty in animals was studied and their somatic development was assessed. Further studies were conducted in 6-month-old sexually mature rats. The results were compared with the corresponding parameters in intact animals. Pubertal stress delayed sexual maturation in females and decreased weight gain in males. In adult animals of both sexes, pubertal stress did not change testosterone levels or the weight and morphology of the gonads significantly, except for minor vacuolation of the spermatogenic epithelium. The spermatogenesis index in the experimental group was significantly lower than in the control, due to a decrease in the number of late spermatids. Pubertal stress led to a 25.9% decrease in the number of spermatozoa in epididymal washes, an increase in the number of their pathological forms and a 2.4-fold slowdown in oxidative-reductive processes in spermatozoa. The content of malonic dialdehyde increased in the testes and ovaries, which indicates the activation of lipid peroxidation. Thus, chronic pubertal stress led to a decrease in the reproductive potential of male rats. Females are less susceptible to the negative effects of pubertal stress.