Intensity Of Oxidative Stress Research Articles

#612 Serum citrulline level is associated with oxidative stress and chronic kidney disease progression

Abstract Background and Aims Citrulline, an α-amino acid crucial for the urea cycle and nitric oxide production, plays a protective role against free radicals and is indirectly related to protein metabolism. It is synthesized in the intestine and efficiently absorbed by the proximal renal tubules, where it is converted to urea via arginine. Although citrulline has multiple physiological effects, its involvement in the progression of chronic kidney disease (CKD) has not been explored. This cross-sectional study aimed to investigate the relationship between serum citrulline levels, CKD progression, and markers of oxidative stress. Method A total of 135 subjects were enrolled in this cross-sectional study. This cohort included 30 relatively healthy individuals who constituted the control group and 105 CKD patients who were categorized according to their estimated glomerular filtration rate (eGFR). We measured serum citrulline concentrations along with markers of oxidative stress, including paraoxonase 1 (PON-1), myeloperoxidase (MPO), and malondialdehyde (MDA), using the spectrophotometric method. Data were expressed as mean (M) and standard deviation (SD) or median and interquartile range [Me (Q25-Q75)] according to the data distribution and compared with the Kruskal-Wallis test. Spearmen correlation test was performed to evaluate the correlation between the studied data. Results Our findings revealed a significant increase in citrulline and MDA concentrations and MPO activity and a significant decrease in PON-1 in the CKD group compared with the control group. Moreover, a significant association emerged between serum citrulline levels and the severity of CKD, as determined by eGFR. Specifically, patients in advanced CKD stages exhibited elevated serum citrulline concentrations in contrast to those in earlier stages (Table 1). Furthermore, a significant correlation was established between serum citrulline and oxidative stress markers, with higher citrulline levels positively associated with increased concentrations of MDA (r = 0.46, p = 0.002) and heightened MPO activity (r = 0.85, p < 0.001), and demonstrating an inverse relationship with PON-1 in CKD stages 1-2 and 5 (r = -0.64, p < 0.001 and r = -0.47, p = 0.004, respectively). Conclusion This cross-sectional study suggests that serum citrulline level is associated with both CKD progression and oxidative stress intensity in patients with CKD. These findings highlight the potential role of citrulline as a biomarker for CKD progression and its implications in the management of oxidative stress in CKD. Further research is warranted to elucidate the underlying mechanisms and explore the therapeutic potential of citrulline supplementation in CKD patients.

THE INFLUENCE OF QUERCETIN ON THE PRODUCTION OF REACTIVE OXYGEN-NITROGEN FORMS IN THE STRUCTURE OF THE INTERSTITIAL SPACE OF RAT TESTICLES WITH LONG-TERM EFFECT OF TRIPTORELIN

Quercetin is a flavonoid commonly found in fruits, vegetables, and seeds. Flavonoids can help prevent cardiovascular diseases, reduce the risk of degenerative brain processes and cancer. Studies have shown that blocking the synthesis of luteinising hormone can lead to oxidative stress in the liver, heart, and salivary glands of rats. The purpose of this study was to assess alterations in the interstitial space of rat testes, identify sources of nitric oxide production, and measure the intensity of oxidative stress in the testes during long-term experimental central blocking of luteinising hormone synthesis by tryptorelin. The study was conducted on 15 sexually mature male white rats. The animals were divided into two groups. The first group (control) received a subcutaneous injection of 0.9% sodium chloride solution. The second group (experimental) received a subcutaneous injection of tryptorelin at a dose of 0.3 mg/kg of active ingredient for 365 days, with simultaneous addition of quercetin to the diet, which was administered orally through a gastric tube three times a day. Total nitric oxide production was assessed by measuring the activity of total NO synthase (gNOS). The activity of gNOS was determined by the increase in nitrite (NO2-) after incubation in Tris-buffered saline. The nitrite concentration was determined using the Gris-Ilosvay reagent at a wavelength of 540 nm. The activity of the inducible (iNOS) and constitutive (cNOS) isoforms was also determined using a selective iNOS inhibitor, aminoguanidine hydrochloride. The production of superoxide anion radical (O2--) was measured by the increase in the formation of diformazan resulting from the reaction of O2-- with nitroblue tetrazolium after incubation in a buffered solution containing sodium hydroxide. The administration of quercetin mitigates the adverse effects of tryptorelin on the structural and functional components of the connective tissue in the rat testes. This effect is observed on day 365 and is characterised by fibrosis and impaired nitric oxide production by constitutive isoforms of NO synthase.

Assessment of the oxidative stress intensity and the integrity of cell membranes under the manganese nanoparticles toxicity in wheat seedlings

A response to manganese nanoparticles was studied in seedlings of two wheat cultivars and a model system of plant cell membranes. Nanoparticles at concentrations of 125 and 250 mg/ml were applied foliar. The application of NPs enhanced the content of Mn in plant cells, indicating its penetration through the leaf surface. The stressful effect in the plant cells was estimated based on changes in the activity of antioxidant enzymes, content of chlorophylls and starch. MnNPs evoked no significant changes in the leaf morphology, however, an increase in enzyme activity, starch accumulation, and a decrease in chlorophyll synthesis indicated the stress occurrence. Moreover, a rise in the electrokinetic potential of the chloroplast membrane surface and the reconstruction of their hydrophobic parts toward an increase in fatty acid saturation was found.

Redox Biomarkers and Matrix Remodeling Molecules in Ovarian Cancer.

Ovarian cancer (OC) has emerged as the leading cause of death due to gynecological malignancies among women. Oxidative stress and metalloproteinases (MMPs) have been shown to influence signaling pathways and afflict the progression of carcinogenesis. Therefore, the assessment of matrix-remodeling and oxidative stress intensity can determine the degree of cellular injury and often the severity of redox-mediated chemoresistance. The study group comprised 27 patients with serous OC of which 18% were classified as Federation of Gynecology and Obstetrics (FIGO) stages I/II, while the rest were diagnosed grades III/IV. The control group comprised of 15 ovarian tissue samples. The results were compared with genetic data from The Cancer Genome Atlas. Nitro-oxidative stress, inflammation and apoptosis biomarkers were measured colorimetrically/fluorometrically or via real-time PCR in the primary ovarian tumor and healthy tissue. Stratification of patients according to FIGO stages revealed that high-grade carcinoma exhibited substantial alterations in redox balance, including the accumulation of protein glycoxidation and lipid peroxidation products. TCGA data demonstrated only limited prognostic usefulness of the studied genes. In conclusion, high-grade serous OC is associated with enhanced tissue oxidative/nitrosative stress and macromolecule damage that could not be overridden by the simultaneously augmented measures of antioxidant defense. Therefore, it can be assumed that tumor cells acquire adaptive mechanisms that enable them to withstand the potential toxic effects of elevated reactive oxygen species.

The Neuroprotective Effects of Curcumin Nanoparticles on The Cerebral Ischemia-Reperfusion Injury in The Rats-The Roles of The Protein Kinase RNA-Like ER Kinase/Extracellular Signal-Regulated Kinase and Transcription Factor EB proteins.

Reduction of cerebral ischemia-reperfusion injury (IRI)/re-oxygenation injury, is defined as the paradoxical exacerbation of the cellular dysfunction and death, following restoration of the blood flow to previously ischemic tissues. The re-establishment of blood flow is essential to salvage the ischemic tissues. As a result, the treatment of IRI with novel therapies, which have fewer side effects, are of great importance. Therefore, this study aimed to investigate the effects of curcumin nanoparticle (CN) pre-treatment on the cerebral I/R rat model. In this experimental study, CN was administered to rats orally five days before the bilateral common carotid artery occlusion (BCCAO) and continued for three days. The intensity of oxidative stress, the activities of antioxidant enzymes, glutathione (GSH) content, the activity of mitochondrial enzymes, including succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and lactate dehydrogenase (LDH), curcumin bioavailability, pERK/ERK expression ratio and TFEB protein were studied. Data analysis was performed using Graphpad Prism V.8 software, one-way analysis of variance (ANOVA) with the statistical package for the social sciences (SPSS V.26 software). Cerebral IRI-damage significantly increased the oxidative stress (P=0.0008) and decreased the activity of the antioxidant enzymes including catalase (CAT) (P<0.001), super oxide dismutase (SOD) (P<0.001), reduced GSH (P<0.001), mitochondrial enzymes, pERK/ERK expression ratio (P=0.002) and TEFB protein (P=0.005) in rats' brains. In addition, the pre-treatment of the rats with CN resulted in a decrease in the reactive oxygen species (ROS), and an increase in the activities of antioxidants and mitochondrial enzymes. This in turn up-regulated the pERK/ERK expression ratio and TEFB expression. CN has neuroprotective effects on the cerebral IRI condition due to its antioxidant properties and is able to overexpress the pERK and TFEB proteins; thus, it can be considered as a suitable treatment option during and after the incidence of stroke.

Neuroprotective Effects and Cognitive Enhancement of Allomargaritarine in 5xFAD Alzheimer's Disease Mice Model

Here, we report the results of an investigation of the neuroprotective effects of securinine with tryptamine conjugate-allomargaritarine (2b), previously selected as the leading compound among a wide range of natural derivatives. 2b was synthesized from securinine using various Lewis acids as catalysts. In addition to the antioxidant and cytoprotective properties previously shown for 2b, in this work,&lt;em&gt; in vitro&lt;/em&gt; analysis of the biological activity of the compound demonstrated that this conjugate is also able to influence the primary pathogenetic mechanism of Alzheimer's disease - proteinopathy, modulating the homeostasis of β-amyloid peptide. In particular, it was found that 2b is an effective inhibitor of β-secretase 1 - an enzyme responsible for initiating the generation of pathological forms of β-amyloid peptide, as well as directly preventing the pathological aggregation of Aβ&lt;sub&gt;1-42&lt;/sub&gt;. As a compound with a promising biological activity profile found &lt;em&gt;in vitro&lt;/em&gt;, 2b has also demonstrated excellent neuroprotective effects on the &lt;em&gt;in vivo&lt;/em&gt; 5xFAD Alzheimer's disease transgenic mice model. Thus, 2b effectively restored cognitive dysfunction: short-term and long-term episodic and spatial memory, which in the &lt;em&gt;post-mortem&lt;/em&gt; studies was also accompanied by a decrease in the number of amyloid deposits and the intensity of oxidative stress in brain samples. These results provide an opportunity to draw a line under years of research on the neuroprotective potential of 2b as a viable therapy for Alzheimer's disease.

Oxidative and nitrosative stress — the leading mechanisms of chronic pancreatitis and chronic obstructive pulmonary disease interaction and inducers of their progression

Background. The frequency of chronic pancreatitis (CP) comorbidity with chronic obstructive pulmonary disease (COPD) has significantly increased recently. It may be accompanied by changes in oxidant-antioxidant homeostasis and activates a cascade of reactions of mutual burdening of these pathologies. The purpose of the current research was to evaluate the intensity of lipid peroxidation, oxidative modification of proteins and the state of individual factors of the antioxidant defense system in the development and course of CP, depending on the comorbid COPD. Materials and methods. Three hundred and seventeen patients were examined, including 62 patients with CP alone (group 1), 132 CP patients with comorbid COPD (group 2), 123 patients with COPD alone (group 3). The content in blood of isolated double bonds in compounds, conjugated dienes, ketodienes and conjugated trienes, malonic aldehyde, nitrites/nitrates, reduced glutathione, the activity of catalase, glutathione-S-transferase, glutathione peroxidase were evaluated in all patients. Results. In CP patients with comorbid COPD, the maximum oxidative stress intensity among the compared groups was registered. There was a reliable increase in the content of malonic aldehyde — by 2.0 times (p &lt; 0.05), isolated double bonds — by 2.2 times (p &lt; 0.05), conjugated dienes — by 1.9 times (p &lt; 0.05), ketodienes and conjugated trienes — by 1.9 times (p &lt; 0.05), nitrites/nitrates — by 2.6 times (p &lt; 0.05). A reliable decrease in reduced glutathione content of erythrocytes was detec­ted: in group 1 — by 1.5 times, in group 2 — by 1.9 times (p &lt; 0.05), in group 3 — by 1.2 times (p &lt; 0.05). The compensatory increase in the activity of glutathione-S-transferase, glutathione peroxidase and blood catalase was revealed: in group 1 — by 1.3, 1.2 and 1.5 times (p &lt; 0.05); in group 2 — by 1.5, 1.3 and 1.8 times (p &lt; 0.05), in group 3 — by 1.2, 1.2 and 1.4 times, respectively (p &lt; 0.05). Conclusions. The comorbid course of CP and COPD is accompanied by the maximum intensity of oxidative and nitrosative stress compared to the isolated course of the disease. An increase was detected in intermediate and final metabolites of peroxide oxidation in the blood, oxidative modification of proteins, nitrites/nitrates in the blood against the background of a deep imbalance of antioxidant defense factors, an increase in ceruloplasmin content in the blood, which requires the administration of antioxidant agents to correct detected disorders and prevent the progression of both comorbid diseases.

Monitoring Alzheimer’s disease via ultraweak photon emission

In an innovative experiment, we detected ultraweak photon emission (UPE) from the hippocampus of male rat brains and found significant correlations between Alzheimer's disease (AD), memory decline, oxidative stress, and UPE intensity. These findings may open up novel methods for screening, detecting, diagnosing, and classifying neurodegenerative diseases, particularly AD. The study suggests that UPE from the brain's neural tissue can serve as a valuable indicator. It also proposes the development of a minimally invasive brain-computer interface (BCI) photonic chip for monitoring and diagnosing AD, offering high spatiotemporal resolution of brain activity. The study used a rodent model of sporadic AD, demonstrating that STZ-induced sAD resulted in increased hippocampal UPE, which was associated with oxidative stress. Treatment with donepezil reduced UPE and improved oxidative stress. These findings support the potential utility of UPE as a screening and diagnostic tool for AD and other neurodegenerative diseases.

Oxidative Stress in Pregnancy.

Recent years have seen an increased interest in the role of oxidative stress (OS) in pregnancy. Pregnancy inherently heightens susceptibility to OS, a condition fueled by a systemic inflammatory response that culminates in an elevated presence of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the circulatory system. The amplified OS in pregnancy can trigger a series of detrimental outcomes such as underdevelopment, abnormal placental function, and a host of pregnancy complications, including pre-eclampsia, embryonic resorption, recurrent pregnancy loss, fetal developmental anomalies, intrauterine growth restriction, and, in extreme instances, fetal death. The body's response to mitigate the uncontrolled increase in RNS/ROS levels requires trace elements that take part in non-enzymatic and enzymatic defense processes, namely, copper (Cu), zinc (Zn), manganese (Mn), and selenium (Se). Determination of ROS concentrations poses a challenge due to their short half-lives, prompting the use of marker proteins, including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), and glutathione (GSH). These markers, indicative of oxidative stress intensity, can offer indirect assessments of pregnancy complications. Given the limitations of conducting experimental studies on pregnant women, animal models serve as valuable substitutes for in-depth research. This review of such models delves into the mechanism of OS in pregnancy and underscores the pivotal role of OS markers in their evaluation.

Characterization of the Spectrum of Mitochondrial DNA Nucleotide Substitutions in Human Populations in High Altitude Environments

Using phylogenetic analysis of the nucleotide sequences of whole mitochondrial genomes (mtDNA), the spectra of germinal nucleotide substitutions (on the L-chain of mtDNA) were reconstructed in highland populations of the Pamirs and Tibet in comparison with regional indigenous groups of West Asia, Northeast Siberia, and South Siberia. No differences were found in the distribution of nucleotide substitution frequencies in the mtDNA spectra depending on the population distribution by altitude. Pyrimidine transitions dominate in all mtDNA spectra, and T → C substitutions are the most frequent among them. Next in frequency in most regional groups are A → G substitutions, but in the Pamir and northeast Asian groups G → A substitutions are prevalent. Of the transversions in all populations studied C → A replacements were found to be predominant, except for the Tibetan one, where A → C substitutions are more frequent. The lack of differences in the distribution of mtDNA mutations in high-altitude and non-highland populations indicates that the structure of mtDNA spectra in human populations is independent of the oxidative stress intensity in mitochondria.

Protective effect of the extract from Aronia melanocarpa L. berries against cadmium-induced oxidative stress in the kidney: A study in an in vivo experimental model

The destructive impact of cadmium (Cd) on the oxidative/antioxidative status of the kidney, as well as the possible beneficial effect of co-administration of a 0.1% aqueous extract from Aronia melanocarpa L. berries (AM), were studied in a rat model of low-level and moderate general population exposure to this heavy metal (1 and 5 mg Cd/kg feed, respectively, for up to 24 months). Total antioxidative status (TAS) of the kidney and the main indices of the enzymatic (superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase) and non-enzymatic (reduced glutathione and thioredoxin) antioxidative barrier were assessed. The total oxidative status (TOS) and concentrations of hydrogen peroxide, xanthine oxidase, myeloperoxidase, and oxidized glutathione were measured as markers of oxidative status. The oxidative stress index (OSI) was calculated (TOS/TAS) to estimate the intensity of oxidative stress in the kidney. The exposure to Cd, dose- and duration-dependently, weakened the enzymatic and non-enzymatic antioxidative potential of the kidney leading to a decrease in its TAS, as well as enhanced oxidative status of this organ resulting in the development of oxidative stress. The administration of AM during the low-level and moderate intoxication with Cd significantly protected from this xenobiotic-induced disruption of the oxidative/antioxidative balance and development of oxidative stress in the kidney. In summary, even low-level long-term exposure to Cd may result in the occurrence of oxidative stress in the kidney, whereas supplementation with chokeberry products may improve the oxidative/antioxidative balance preventing oxidative stress in this organ.

Overexpression of Lias Gene Alleviates Cadmium-Induced Kidney Injury in Mice Involving Multiple Effects: Metabolism, Oxidative Stress, and Inflammation.

Oxidative stress is an important mechanism underlying toxicity induced by cadmium (Cd) exposure. However, there are significant differences of the antioxidant baseline in different populations. This means that different human has different intensity of oxidative stress in vivo after exposure to toxicants. LiasH/H mouse is a specific model which is created by genetically modifying the Lias 3'-untranslated region (3'-UTR). LiasH/H mice express high levels of LA and have high endogenous antioxidant capacity which is approximately 150% higher than wild-type C57BL/6J mice (WT, Lias+/+). But more importantly, they have dual roles of metal chelator and antioxidant. Here, we applied this mouse model to evaluate the effect of endogenous antioxidant levels in the body on alleviating Cd-induced renal injury including Cd metabolism, oxidative stress, and inflammation. In the experiment, mice drank water containing Cd (50mg/L), for 12weeks. Many biomarkers of Cd metabolism, oxidative stress, inflammation, and major pathological changes in the kidney were examined. The results showed overexpression of the Lias gene decreased Cd burden in the body of mice, mitigated oxidative stress, attenuated the inflammatory response, and subsequent alleviated cadmium-induced kidney injury in mice.

Immunological Reactivity and Intensity of Oxidative Stress in Stable Coronary Artery Disease

The aim. To analyze the relationship between immune response factors and the intensity of oxidation of lipoproteins and proteins in patients with stable coronary artery disease (CAD) to clarify the pathogenesis of coronary atherosclerosis.&#x0D; Materials and methods. A total of 179 patients with stable CAD of II-IV functional class, mean age 56 (49-62) years (main group) and 30 healthy individuals, mean age 49 (45-53) years (control group) were examined. The material for immunological research was peripheral venous blood. To determine the indicators of immunity, flow laser cytometry and enzyme-linked immunosorbent assay were used. Spectrophotometric and fluorometric methods were used to determine the levels of intermediate and final oxidation products of lipids and proteins, as well as antioxidant protection enzymes in the blood serum and in atherogenic lipoproteins.&#x0D; Results. A direct relationship between the activity of lipoprotein peroxidation and protein oxidation with a cell-type immune response and immune inflammation was revealed.&#x0D; Conclusions. The high intensity of lipid peroxidation and protein oxidation in patients with stable CAD (stable angina pectoris) is combined with significant activation of the T-cell component of the immune response (in terms of the ratio of helper and cytotoxic subpopulations of T-lymphocytes, high concentrations of pro-inflammatory cytokines, the state of the CD40/CD40L system, the level of expression of the CD95 apoptosis marker on cells), which indicates interdependence of T-cell immunity and oxidative stress in the pathogenesis of atherosclerosis. The dependence of the hyperproduction of pro-inflammatory cytokines by mononuclear blood cells on free radical oxidation of proteins, peroxidation of apoB proteins and the intensity of antiperoxide protection (catalase and superoxide dismutase enzymes) in patients with stable CAD indicates a contribution to the presence of oxidative stress and the development of immune inflammation. A comprehensive study of the factors of immunological reactivity, the violation of which can lead to the development of immunopathological reactions, and the intensity of oxidation of lipoproteins and proteins in patients with stable CAD helps to clarify the pathogenetic relationship between chronic immune inflammation, endothelial dysfunction and oxidative stress, and also substantiates the expediency of general therapeutic approaches to the treatment of CAD.

Short-Term Pretreatment with Melatonin Increases the Resistance of&#x0D; Barley Plants to the Subsequent Action of Cadmium

The effect of short-term and long-term root treatment with melatonin on growth parameters, photochemical activity of PSII, content of basic photosynthetic pigments, lipid peroxidation, and accumulation ofinorganic ions in barley plants under the action of cadmium chloridewas studied. It was shown for the first time that the protectiveeffect of phytomelatonin during short-term treatment is manifested ina decrease in the toxic effect of cadmium on the content ofphotosynthetic pigments and the accumulation of cadmium ions in theshoots and roots of barley plants. The protective effect of melatoninis based on its ability to reduce the intensity of oxidative stress bymaintaining the level of carotenoids and increasing the activity ofantioxidant enzymes. The effectiveness of short-term use of melatoninin a number of indicators exceeds its protective effect from long-termexposure. The data obtained indicate the possibility of usingmelatonin as a substance that induces the state of plant priming uponsubsequent exposure to cadmium.

Harmfulness of prooxidants in bronchopulmonary dysplasia in preterm children

Introduction. Oxidative stress can be defined as the imbalance of the redox state of a certain system including living one (organelle, cell, organ/tissue), which excessively produces reactive oxygen and/or reactive nitrogen species (ROS/RNS) that exceed the capacity of the antioxidant defense system, which have the ability to slow down or even prevent the oxidative damage of macromolecules. Oxidative stress is a pathogenic mechanism of a large variety of diseases, including pulmonary one. Material and methods. 81 preterm born children included in the study were divided into the main group – preterm children with bronchopulmonary dysplasia (BPD), and the control group – preterm children without BPD. The comparison groups were prospectively evaluated clinical, instrumental and laboratory (TPA, prooxidant-antioxidant balance, nitric oxide metabolistes and MDA). Data were statistically analyzed using Microsoft Excel, MedCalc and SPSS and Contingency Table Analysis as a way to evaluate the performance of a diagnostic test. Results. In preterm children with BPD were found to be decreased by 29% (p &lt; 0.001) the prooxidant-antioxidant balance (PAB) and the nitric oxide metabolistes (NO) level by 12% (p &lt; 0.001) compared to children in the control group. The assessment of tissue oxidative damage markers revealed a significant 62% (p &lt; 0.001) increase in malonic dialdehyde (MDA) content and a 4.86-fold (p &lt; 0.001) increase in total prooxidant activity (TPA) in children with bronchopulmonary dysplasia compared to children in the control group. Our study confirms that TPA, PAB, MDA and NO values are reliable markers of hypoxic tissue damage at children with bronchopulmonary dysplasia and can be recommended for assessing the intensity of oxidative stress. Conclusions. Pulmonary bronchodysplasia is characterized by the imbalance of prooxidant-antioxidant processes with the exacerbation of prooxidant ones that trigger the oxidative/nitrosative stress and the deterioration of vital chemical compounds.

Oxidative stress as the bridge between dyslipidemia and peritoneal ultrafiltration failure: A bi-center cross-sectional cohort study

stress and dyslipidemia are common concerns in patients undergoing peritoneal dialysis (PD) and are associated with adverse clinical outcomes. However, the interplay between these factors and their impact on peritoneal ultrafiltration (UF) remains poorly understood.&#x0D; Methods: In this bi-center cross-sectional cohort study, we examined the relationships between dyslipidemia, oxidative stress, and peritoneal UF in patients undergoing PD. A comprehensive set of oxidative stress markers, lipid profiles, and clinical variables were assessed.&#x0D; Results. Among the 114 patients, aged 55 (48-65) years, with a dialysis vintage of 31 (14-50) months, 76 (66.7%) were diagnosed with dyslipidemia. Patients with dyslipidemia experienced significantly higher proportions of patients with peritoneal UF below 400 mL per day, suggesting ultrafiltration failure (UFF) (χ2 = 4.9, p = 0.02). An elevated D/P creatinine ratio was associated with higher levels of total cholesterol (r = 0.39, p = 0.0005), low-density lipoprotein cholesterol (r = 0.26, p = 0.02), triglycerides (r = 0.33, p = 0.005), and the atherogenic index of plasma (AIP) (r = 0.27, p = 0.01). UF rate displayed a positive correlation with high-density lipoprotein cholesterol (r = 0.31, p = 0.003) and a negative correlation with AIP (r = -0.33, p = 0.004). The ROC analysis revealed that an AIP value exceeding 4.3 could effectively predict UFF, with a sensitivity of 83.3% and a specificity of 73.4%&#x0D; Dyslipidemia was significantly associated with increased intensity of oxidative stress, with elevated malondialdehyde (MDA) (p = 0.0002), oxidative stress index (OSI) (p &lt; 0.0001), and reduced antioxidant markers. UFF was also associated with higher oxidative stress, as indicated by increased MDA (p = 0.005) and OSI (p = 0.0009). Patients with both dyslipidemia and UFF exhibited the highest levels of oxidative stress (p &lt; 0.0001). Taking potential confounders into account in the ANCOVA analysis, a significant interaction effect of dyslipidemia (F = 7.6, p = 0.007) and UF rate (F = 8.6, p = 0.004) on oxidative stress was observed.&#x0D; Conclusion. Dyslipidemia and UFF are independently associated with elevated oxidative stress in PD patients, and their coexistence exacerbates this oxidative burden. Understanding these relationships is crucial for developing interventions to improve clinical outcomes in this population. Targeted therapies addressing oxidative stress and dyslipidemia warrant further investigation.

The effect of quercetin on the morphogenesis of the interstitial space in the testes of rats after 90 days with central blockade of luteinizing hormone

Leydig cells are responsible for the production of testosterone in the male testicles when stimulated by luteinizing hormone (LH). Dysfunction of Leydig cells, which occurs during inflammation or oxidative stress, is one of the main causes of male infertility. The purpose of the study is to determine the effect of quercetin on the microscopic organization of rat testes, nitric oxide production and the intensity of oxidative stress in rat testes on the 90th day of the experiment, during the experimental central deprivation of LH synthesis caused by the administration of triptorelin acetate solution. The experiment was conducted on 20 sexually mature male white rats. Rats were divided into 2 groups of 10 animals in each group: control group (I), group with central deprivation of LH + quercetin synthesis (II). Animals from the group with central blockade of LH synthesis were injected subcutaneously with triptorelin acetate at a dose of 0.3 mg of the active substance per kg and quercetin at 100 mg per kg of body weight 3 times a week, while the control group was injected with saline. Our study of the interstitial space in the testes of white rats showed heterogeneity of macrophage populations and variability of structural and functional parameters. Central blockade of LH synthesis by the administration of treptorelin with the parallel administration of quercitin to the studied animals on the 90th day of the experiment causes changes in the structure of the interstitial space of rat testes, which is characterized by high variability both in the populations of interstitial endocrinocytes and macrophages. Biochemical indicators on the 90th day of the experiment indicate an increase in NO production in conditions of central blocking of the synthesis of luteinizing hormone by more than three times, which is ensured by the activity of the inducible isoform of NOS (iNOS). At the same time, the increase in the activity of iNOS with a decrease in the activity of the arginase pathway leads to the polarization of macrophages according to the pro-inflammatory type. The introduction of quercetin protects the testicular tissue of rats from oxidative damage caused by the administration of triptorelin on the 90th day of the experiment by increasing antioxidant protection and reducing reactive oxygen species in the tissue.

Short-Term Pretreatment with Melatonin Increases the Resistance of Barley Plants to the Subsequent Action of Cadmium

The effect of short-term and long-term root treatment with melatonin on growth parameters, photochemical activity of PSII, content of basic photosynthetic pigments, lipid peroxidation, and accumulation of inorganic ions in barley plants under the action of cadmium chloride was studied. It was shown for the first time that the protective effect of phytomelatonin during short-term treatment is manifested in a decrease in the toxic effect of cadmium on the content of photosynthetic pigments and the accumulation of cadmium ions in the shoots and roots of barley plants. The protective effect of melatonin is based on its ability to reduce the intensity of oxidative stress by maintaining the level of carotenoids and increasing the activity of antioxidant enzymes. The effectiveness of short-term use of melatonin in a number of indicators exceeds its protective effect from long-term exposure. The data obtained indicate the possibility of using melatonin as a substance that induces the state of plant priming upon subsequent exposure to cadmium.

Lias overexpression alleviates pulmonary injury induced by fine particulate matter in mice.

Oxidative stress and inflammation are mechanisms underlying toxicity induced by fine particulate matter (PM2.5). The antioxidant baseline of the human body modulates the intensity of oxidative stress in vivo. This present study aimed to evaluate the role of endogenous antioxidants in alleviating PM2.5-induced pulmonary injury using a novel mouse model (LiasH/H) with an endogenous antioxidant capacity of approximately 150% of its wild-type counterpart (Lias+/+). LiasH/H and wild-type (Lias+/+) mice were randomly divided into control and PM2.5 exposure groups (n = 10), respectively. Mice in the PM2.5 group and the control group were intratracheally instilled with PM2.5 suspension and saline, respectively, once a day for 7 consecutive days. The metal content, major pathological changes in the lung, and levels of oxidative stress and inflammation biomarkers were examined. The results showed that PM2.5 exposure induced oxidative stress in mice. Overexpression of the Lias gene significantly increased the antioxidant levels and decreased inflammatory responses induced by PM2.5. Further study found that LiasH/H mice exerted their antioxidant function by activating the ROS-p38MAPK-Nrf2 pathway. Therefore, the novel mouse model is useful for the elucidation of the mechanisms of pulmonary injury induced by PM2.5.

Antioxidative effect of Periplaneta americana extract on dextran sulfate sodium-induced ulcerative colitis through activation of the Nrf2 signal

Context Periplaneta americana L. (Blattariae) is used as a treatment for ulcerative colitis (UC) in Chinese traditional medicine. Objective To evaluate the antioxidative activity of P. americana whole body ethanol extract (PAE) on UC mice and whether glycine and proline could be used for quality control and identification of active PAE components. Materials and methods NCM460 cells were pre-incubated in PAE, AA-L, AA-M, and AA-H (low, high and medium doses of proline and glycine), then treated with recombinant human TNF-α. The glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen (ROS) levels were determined. UC mice were fed with water containing 2.5% dextran sulfate sodium (w/v) after pre-treatment with different doses of PAE once a day for 7 days. ELISA was used to detect the concentrations of inflammation-related factors. Colon tissues of mice were used to detect the activity of myeloperoxidase (MPO), GSH, MDA, and SOD. Histological changes were observed using H&E staining. The expression of target proteins was determined by western blotting. Results In vivo, PAE treatment reduced the DAI score more than in the model group, restoring the weight and colonic length. It also reduced the severity of colitis, and inflammatory and oxidative stress intensity. Additionally, western blotting showed that the Nrf2 pathway was activated by PAE. In vitro PAE significantly alleviated TNF-α-induced cell damage and oxidative stress, which is relevant to the activation of the Nrf2 pathway. Conclusions PAE may relieve oxidative stress through the Nrf2 signaling pathway, and proline and glycine may be used as active components of its antioxidative stress activity.