Oxidative Markers Research Articles

Sevoflurane anesthesia during late gestation induces cognitive disorder in rat offspring via the TLR4/BDNF/TrkB/CREB pathway.

Sevoflurane (Sevo) is widely used for general anesthesia during pregnancy. Emerging evidence indicates that maternal Sevo exposure can trigger developmental neurotoxicity in the offspring. Nonetheless, the underlying mechanisms need further investigation. Pregnant Sprague-Dawley rats on gestational day 18 were exposed to 3.5% Sevo to induce the rat model of neurotoxicity. TAK-242, a TLR4 inhibitor, was administrated to inhibit the signaling transduction. Hippocampal tissues of rat offspring were harvested for immunohistochemical staining, TUNEL staining, Western blotting, ELISA, and measurement of oxidative stress-related markers. Serum samples were collected to evaluate lipid metabolism-associated factors. Morris water maze was implemented to test the cognitive function of offspring rats. Rat hippocampal neurons were isolated to elucidate the effect of TAK-242 on the BDNF/TrkB/CREB signaling in vitro. The results showed that maternal Sevo exposure during the third trimester induced neuroinflammation, lipid metabolism disturbance, and oxidative stress, and impaired the spatial learning and memory of rat offspring. Sevo upregulated TLR4 and impeded BDNF/TrkB/CREB signaling transduction in the hippocampus of rat offspring; TAK-242 administration reversed these effects. In conclusion, Sevo anesthesia during late gestation impairs the learning and memory ability of rat offspring possibly by promoting neuroinflammation and disturbing lipid metabolism via the TLR4/BDNF/TrkB/CREB pathway.

Insights on the Tunisian Prickly Pear Molasses as a Potential Antifibrotic and Antioxidant Candidate against Lung Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial disease leading to pulmonary damage and respiratory failure. We aimed to investigate the effect of prickly pear molasses (PPM) on an experimental model of pulmonary fibrosis induced by bleomycin (BLM) in Wistar rat. Animals were divided into 5 groups: the control group (G1), the BLM group (G2) and three groups (G3, G4, G5) receiving a single intra-tracheal injection of BLM (4 mg/kg) and PPM (at 2, 4.5 and10 %) that was introduced into the diet one week before BLM injection and continued for 3 weeks. Our phytochemical results revealed significant polyphenol and flavonoid content. LCMS analysis revealed the presence of Sinapinic acid, t-ferulic acid, t-cinnamic acid, Caffeic acid, gallic acid and vallinic acid among others. Our histological study revealed significant decrease in collagen deposition in the groups of rats treated with 4.5 % and 10 % molasses compared to BLM group. Oxidative stress in pulmonary tissues was investigated using catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) assays. Treatment with PPM normalized the disturbance in the level of these oxidative markers in G3,G4, G5 compared to G2. In conclusion, PPM exhibit antifibrotic and antioxidant activities in BLM model of lung fibrosis.

Adding Rare Earth Oxide Markers to Polyoxymethylene to Improve Plastic Recycling through Tracer-Based Sorting.

Engineering plastics, such as polyoxymethylene (POM), are high-performance thermoplastics designed to withstand high temperature or mechanical stress and are used in electronic equipment, the automotive industry, construction, or specific household utensils. POM is immiscible with other plastics but due to a low volume of production, no methods were developed to separate it from the residual plastic waste stream. Therefore, POM recycling is minimal despite its high market value. This paper provides a proof of concept for tracer-based sorting (TBS) as a potential solution for increasing the separation efficiency of low-volume, high-quality polymers. For this purpose, yttrium oxide (Y2O3) and cerium (IV) oxide (CeO2) have been embedded into the POM matrix. Mechanical tests of samples at varying concentrations (0.1 to 1000 ppm) of both tracers were conducted, followed by an analysis of detectability and dispersibility using a portable X-ray fluorescence spectrometer (p-XRF), subsequently optimizing detection time and tracer concentration. Finally, an experimental scenario was developed to test the fate and potential recovery of the tracer material after the thermal treatment of plastics. A low detectable concentration, short measurement time, low influence on mechanical parameters of the compound, and low loss ratio after simulated recycling prove Y2O3 to be a suitable tracer for the industrial implementation of TBS.

Ethanol with thioacetamide murine model of alcoholic liver disease identifies hepatic pathways as targets for the human disease

Introduction and ObjectivesHepatic proteome and gut microbiota alterations are known in alcohol-associated hepatitis (AAH). Current animal models sparsely mimic human AAH. We aimed to develop an murine model that closely resembled human AAH. Materials and MethodsMale C57BL/6N mice were pair-fed control/incremental ethanol Lieber-DeCarli diets and thioacetamide (TAA) for 12-weeks to induce AAH. Hepatic proteome was analyzed using LC-MS/MS. Gut-bacteria was determined using 16s-rRNA sequencing. ResultsMice exposed to EtOH+TAA displayed higher expression of liver triglycerides (1.5-fold, p = 0.001), pro-inflammatory (IL6, 1.5-fold, p = 0.002 and TNFα, 1.7-fold, p = 0.01), fibrotic (TGF-β, 2.7-fold, p = 0.01 and Col1α1, 2-fold, p = 0.01) and oxidative markers (GSH and SOD (-1.5 fold, p = 0.004 & 0.005 respectively)) as compared to EtOH alone. Histology of EtOH+TAA liver displayed pericellular liver fibrosis, increased steatosis, and neutrophil infiltration, which resembled human AAH. In the 12wk EtOH+TAA group, Desulfobacteria, Campylobacteria, and Patescibacteria increased by 2-fold (p = 0.02). Pathway combined score (CS, log10) in EtOH+TAA treatment showed upregulated hepatic ethanol oxidation (CS=1.93), fatty acid biosynthesis (CS=2.48), necrosis (CS=1.59), collagen formation (CS=1.28) and hypoxia (CS=0.68) and downregulated fatty acid beta-oxidation (CS=2.37), PPAR signaling (CS=1.35) fatty acid degradation (CS=2.35), bile acid metabolism (CS=1.87), and oxidative phosphorylation (CS=1.50), as observed in human disease. ConclusionsUsing an ethanol-thioacetamide combination in mice results in a faster establishment of AAH with fibrosis than previously known models. Differential protein expression strongly correlates with pathways found altered in human AAH, thus making the model mimic human disease better than other known models., respectively. Thioacetamide (TAA) was administered to enhance liver fibrosis and mimic human AAH.

CYR61/CCN1: A novel mediator of redox response in corneal stromal cells of keratoconus

Keratoconus (KC) is a progressive, multifactorial and ectatic corneal disorder that characterized by steepening thinning of the cornea. It was previously demonstrated that oxidative stress has a strong link with KC progression. However, the molecular mechanism underlying oxidative stress response in KC remains unclear. Hence, the present study analyzed the heterogeneity of response of corneal stromal cells (CSCs) to oxidative stress in order to further illustrate how oxidative shape the pathophysiology of KC. Single-cell transcriptomics analysis revealed that CSCs demonstrated significant higher oxidative stress score in the KC group compared to the Ctrl group. The expression of oxidative markers verified by experiments illustrated elevated oxidative stress levels and insufficient antioxidant levels in CSCs of KC. In further single-cell transcriptomics analysis, we identified CYR61 to distinguish different subgroups of CSCs responding to oxidative stress. The cornea stroma cells in KC could be differentiated into CYR61high cells and CYR61low cells. Of note, the CYR61high cells showed lower score in collagen production process and higher score in collagen catabolic process. Further experiments illustrated that CYR61 was elevated in KC and associated with collagen production.

Serum oxidative stressors levels and association of mtDNA variants with type 2 diabetes mellitus in the Central India population

BackgroundThe mitochondrial genome has a high rate of mutability which plays a major role in pathogenic mutations. These mutations are implicated with mitochondrial dysfunction increasing the vulnerability to Diabetes Mellitus (DM). AimThe study aimed to evaluate the changes in oxidative markers and analyse the specific mitochondrial DNA variants that contributed to DM in the central Indian population. MethodTo assess mitogenomic alteration, Sanger sequencing was used to identify the single nucleotide polymorphisms (SNPs) or variants, while ELISA kits were used to evaluate oxidative stress. ResultsThe levels of 8-Hydroxy-2-deoxyguanosine (8-OHdG) and Malondialdehyde (MDA) in type 2 diabetes mellitus (T2DM) were significantly higher than in healthy individual (HI). In T2DM (3371.80 ± 1110.7 pg/ml) the levels of 8-OHdG were significantly greater and were found to be nine times higher compared to the control group (P < 0.001). Additionally, MDA level which is indicative of lipid peroxidation, in the diabetic groups (39.34 ± 23.05 ng/ml) contributed to 18 times higher than the control groups (2.16 ± 2 ng/ml). Moreover, 52 variants were found in our population, among which C10400T variants were significantly prevalent and clustered with the A10398G. These variants confirmed a strong association, on analysis for linkage disequilibrium (r2), with a slightly higher r2 value in the T2DM group (0.92) compared to controls (0.85), indicating a stronger link with diabetes. According to multivariate regression analysis, variants associated with the mitogenome such as C16192T (CI: 0.004 to 1.30, p = 0.028) were found to play a protective role against T2DM. Furthermore, A3384G and G16129A may contribute to the protective role against the risk of developing diabetes. ConclusionThe study demonstrates that diabetic patients are more vulnerable to certain mtDNA variants, directly linked to increased hyperglycemia. Elevated free radical-mediated oxidative stress likely affects these mtDNA variants.

Phycocyanin attenuates skeletal muscle damage and fatigue via modulation of Nrf2 and IRS-1/AKT/mTOR pathway in exercise-induced oxidative stress in rats.

Prolonged strenuous exercise induces oxidative stress, leading to oxidative damage, skeletal muscle fatigue, and reduced exercise performance. The body compensates for oxidative stress through antioxidant actions, while related enzymes alone may not overcome excessive oxidative stress during prolonged strenuous exercise. Phycocyanin is an important antioxidant supplement derived from blue-green algae, which may be helpful in this type of situation. This study determined the effects of phycocyanin on exercise performance from prolonged strenuous exercise. Forty Sprague Dawley male rats were divided into 5 groups (n = 8 /group); Control group (C), Exercise group (E), and Exercise with supplement groups receiving low dose (Phycocyanin = 100 mg/kg BW; ELP) and high dose (Phycocyanin = 200 mg/kg BW; EHP) or vitamin C (Vitamin C = 200 mg/kg BW; VC). Phycocyanin was found to decrease oxidative damage markers, muscle fatigue, and muscle atrophy through the activated AKT/mTOR pathway. This was also found to have greater increases in antioxidants via Nrf2 signaling and increases ATP synthesis, GLUT4 transporters, and insulin signaling due to increased IRS-1/AKT signaling. In conclusion, phycocyanin was found to reduce oxidative damage and muscle atrophy, including an increase in insulin signaling in skeletal muscles leading to increased exercise performance in rats.

Mitochondrial dysfunction and oxidative stress in selective fetal growth restriction

IntroductionPlacental dysfunction is the primary cause of selective fetal growth restriction (sFGR), and the specific role of mitochondria remains unclear. This study aims to elucidate mitochondrial functional defects in sFGR placentas and explore the roles of mitochondrial genomic and epigenetic alterations in its pathogenesis. MethodsThe placental villi of MCDA twins with sFGR were collected and the morphology and number of mitochondria were observed by transmission electron microscopy. Meanwhile, the levels of reactive oxygen species (ROS), ATP and oxidative damage markers were assessed. Mitochondrial DNA (mtDNA) copy number detection, targeted sequencing and methylation sequencing were performed. The expression of placental cytochrome c oxidase subunit I (COX I) and mitochondrial long non-coding RNAs (lncRNAs) were evaluated by Western blotting and qPCR. ResultsCompared with placentae from normal fetuses, pronounced mitochondrial damage within cytotrophoblast was revealed in sFGR placentae, alongside augmented mitochondrial number in syncytiotrophoblast. Enhanced oxidative stress in these placentae was evidenced by elevated markers of oxidative damage, accompanied by increased ROS production and diminished ATP generation. In sFGR placentae, a notable rise in mitochondrial copy number and one heterozygous mutation in the MT-RNR2 gene were observed, along with decreased COX Ⅰ levels, increased lncND5, lncND6, lncCyt b, and MDL1 synthesis, and decreased RMRP synthesis. DiscussionFindings collectively confirmed an exacerbation of oxidative stress within sFGR placentae, coinciding with mitochondrial dysfunction, compromised energy production, and ultimately the failure of compensatory mechanisms to restore energy balance, which may result from mutations in the mitochondrial genome and abnormal expression of epigenetic regulatory genes.

Combined effects of vitamin D3 and dioxopiperidinamide derivative on lipid homeostasis, inflammatory pathways, and redox imbalance in non-alcoholic fatty liver disease in vivo zebrafish model.

Liver damage and metabolic dysfunctions, the defining features of non-alcoholic fatty liver disease (NAFLD), are marked by inflammation, oxidative stress, and excessive hepatic fat accumulation. The current therapeutic approaches for NAFLD are limited, necessitating exploring novel treatment strategies. Dioxopiperidinamide derivatives, particularly DOPA-33, have shown effective anti-inflammatory and antioxidant properties, potentially offering therapeutic benefits against NAFLD. This study investigated the combined potential of vitamin D3 (Vit D3) and DOPA-33 in treating NAFLD. The network pharmacology analysis identified key NAFLD targets modulated by Vit D3 and DOPA-33, emphasizing their potential mechanisms of action. In NAFLD-induced zebrafish models, Vit D3 and DOPA-33 significantly reduced hepatic lipid accumulation, oxidative stress, and apoptosis, demonstrating superior efficacy over individual treatments. The treatment also lowered reactive oxygen species (ROS) levels, decreased liver damage, and enhanced antioxidant defense mechanisms. Moreover, behavioral analyses showed improved locomotion and reduced weight gain in treated zebrafish. Biochemical analyses revealed lower triglycerides (TG) and glucose levels with improved oxidative markers. Furthermore, histological analyses indicated reduced hepatic steatosis and inflammation, with decreased expression of lipogenesis-related genes and inflammatory mediators. Finally, high-performance liquid chromatography (HPLC) confirmed a significant reduction in hepatic cholesterol levels, indicating the effectiveness of the combination therapy in addressing key NAFLD-related dyslipidemias. These findings suggest that Vit D3 + DOPA-33 targets pathways involved in lipid metabolism, inflammation, and oxidative stress by offering a promising therapeutic approach for NAFLD.

Ccn2 Deletion Reduces Cardiac Dysfunction, Oxidative Markers, and Fibrosis Induced by Doxorubicin Administration in Mice.

Cellular Communication Network Factor 2 (CCN2) is a matricellular protein implicated in cell communication and microenvironmental signaling. Overexpression of CCN2 has been documented in various cardiovascular pathologies, wherein it may exert either deleterious or protective effects depending on the pathological context, thereby suggesting that its role in the cardiovascular system is not yet fully elucidated. In this study, we aimed to investigate the effects of Ccn2 gene deletion on the progression of acute cardiac injury induced by doxorubicin (DOX), a widely utilized chemotherapeutic agent. To this end, we employed conditional knockout (KO) mice for the Ccn2 gene (CCN2-KO), which were administered DOX and compared to DOX-treated wild-type (WT) control mice. Our findings demonstrated that the ablation of CCN2 ameliorated DOX-induced cardiac dysfunction, as evidenced by improvements in ejection fraction (EF) and fractional shortening (FS) of the left ventricle. Furthermore, DOX-treated CCN2-KO mice exhibited a significant reduction in the gene expression and activation of oxidative stress markers (Hmox1 and Nfe2l2/NRF2) relative to DOX-treated WT controls. Additionally, the deletion of Ccn2 markedly attenuated DOX-induced cardiac fibrosis. Collectively, these results suggest that CCN2 plays a pivotal role in the pathogenesis of DOX-mediated cardiotoxicity by modulating oxidative stress and fibrotic pathways. These findings provide a novel avenue for future investigations to explore the therapeutic potential of targeting CCN2 in the prevention of DOX-induced cardiac dysfunction.

Nanostructure-assisted drought tolerance in olive trees (Olea europaea L.): the role of Fe2O3-graphitic carbon.

Olive trees are known as one of the most iconic crops in the world. Considering the increasing water deficit worldwide, implementing some profitable and empirical strategies can be inevitable upon exposure to drought stress. Therefore, the present study aimed at clarifying the beneficial role of exogenously foliar application of Fe2O3 modified carbon nitride nanostructures (control, FeSO4, C3N4 and Fe2O3/g-C3N4) to "Shengeh" olive cultivars grown at different watering levels (100, 75, and 50% ET) in two experimental years (2022 and 2023) and the pomological attributes, physiological and biochemical changes happening in the treated leaves and fruits were discussed. The results indicated that drought stress caused a significant decline in pomological attributes in this experiment, and treatments could remarkably make up for this damage. Overall, Fe2O3/g-C3N4 outperformed as compared FeSO4 and C3N4 alone, which were also efficacious in conferring tolerance to the water deficit stress. Conversely, severe drought stressed-olive fruits showed higher oil content percent in the fresh matter and water use efficiency (WUE) in oil by 30% and 52.5%, respectively, as an average of results of two years, and after Fe2O3/g-C3N4, these features in olive plants subjected to severe drought improved by an average of 35% over two years. Ca2+ and K+ in olive plants under severe drought stress declined by 50% and 83% in 2022 and 46% and 24% in 2023, while Na+ increased in the plants exposed to 50%ET stress by 48% and 57% in two successive experimental years respectively. The application of Fe2O3/g-C3N4 remarkably improved the contents of Ca2+ and K+ by 101.5% and 369%, respectively, as an average of two years. Conversely, this beneficial treatment led to a significant decline in Na+ levels by 30% in 2022 and 2% in 2023 under stressful conditions. Moreover, it decreased the 'osmolytes' content, caused a smaller decline in chlorophyll levels, and resulted in higher relative water content occurring in the treated olive leaves. The reduction of oxidative markers was a result of the increased enzymatic activity after the use of Fe2O3/g-C3N4. Therefore, this treatment is a promising strategy to achieve improved resistance in olive plants in the future.

Identification and validation of oxidative stress-related diagnostic markers for recurrent pregnancy loss: insights from machine learning and molecular analysis.

It has been recognized that oxidative stress (OS) is implicated in the etiology of recurrent pregnancy loss (RPL), yet the biomarkers reflecting oxidative stress in association with RPL remain scarce. The dataset GSE165004 was retrieved from the Gene Expression Omnibus (GEO) database. From the GeneCards database, a compendium of 789 genes related to oxidative stress-related genes (OSRGs) was compiled. By intersecting differentially expressed genes (DEGs) in normal and RPL samples with OSRGs, differentially expressed OSRGs (DE-OSRGs) were identified. In addition, four machine learning algorithms were employed for the selection of diagnostic markers for RPL. The Receiver Operating Characteristic (ROC) curves for these genes were generated and a predictive nomogram for the diagnostic markers was established. The functions and pathways associated with the diagnostic markers were elucidated, and the correlations between immune cells and diagnostic markers were examined. Potential therapeutics targeting the diagnostic markers were proposed based on data from the Comparative Toxicogenomics Database and ClinicalTrials.gov. The candidate biomarker genes from the four models were further validated in RPL tissue samples using RT-PCR and immunohistochemistry. A set of 20 DE-OSRGs was identified, with 4 genes (KRAS, C2orf69, CYP17A1, and UCP3) being recognized by machine learning algorithms as diagnostic markers exhibiting robust diagnostic capabilities. The nomogram constructed demonstrated favorable predictive accuracy. Pathways including ribosome, peroxisome, Parkinson's disease, oxidative phosphorylation, Huntington's disease, and Alzheimer's disease were co-enriched by KRAS, C2orf69, and CYP17A1. Cell chemotaxis terms were commonly enriched by all four diagnostic markers. Significant differences in the abundance of five cell types, namely eosinophils, monocytes, natural killer cells, regulatory T cells, and T follicular helper cells, were observed between normal and RPL samples. A total of 180 drugs were predicted to target the diagnostic markers, including C544151, D014635, and CYP17A1. In the validation cohort of RPL patients, the LASSO model demonstrated superiority over other models. The expression levels of KRAS, C2orf69, and CYP17A1 were significantly reduced in RPL, while UCP3 levels were elevated, indicating their suitability as molecular markers for RPL. Four oxidative stress-related diagnostic markers (KRAS, C2orf69, CYP17A1, and UCP3) have been proposed to diagnose and potentially treat RPL.

Ischemia-reperfusion injury after spinal cord decompressive surgery-An invivo rat model.

Although decompression surgery is the optimal treatment for patients with severe degenerative cervical myelopathy (DCM), some individuals experience no improvement or even a decline in neurological function after surgery, with spinal cord ischemia-reperfusion injury (SCII) identified as the primary cause. Spinal cord compression results in local ischemia and blood perfusion following decompression is fundamental to SCII. However, owing to inadequate perioperative blood flow monitoring, direct evidence regarding the occurrence of SCII after decompression is lacking. The objective of this study was to establish a suitable animal model for investigating the underlying mechanism of spinal cord ischemia-reperfusion injury following decompression surgery for degenerative cervical myelopathy (DCM) and to elucidate alterations in neurological function and local blood flow within the spinal cord before and after decompression. Twenty-four Sprague-Dawley rats were allocated to three groups: the DCM group (cervical compression group, with implanted compression material in the spinal canal, n = 8), the DCM-D group (cervical decompression group, with removal of compression material from the spinal canal 4 weeks after implantation, n = 8), and the SHAM group (sham operation, n = 8). Von Frey test, forepaw grip strength, and gait were assessed within 4 weeks post-implantation. Spinal cord compression was evaluated using magnetic resonance imaging. Local blood flow in the spinal cord was monitored during the perioperative decompression. The rats were sacrificed 1 week after decompression to observe morphological changes in the compressed or decompressed segments of the spinal cord. Additionally, NeuN expression and the oxidative damage marker 8-oxoG DNA were analyzed. Following spinal cord compression, abnormal mechanical pain worsened, and a decrease in forepaw grip strength was observed within 1-4 weeks. Upon decompression, the abnormal mechanical pain subsided, and forepaw grip strength was restored; however, neither reached the level of the sham operation group. Decompression leads to an increase in the local blood flow, indicating improved perfusion of the spinal cord. The number of NeuN-positive cells in the spinal cord of rats in the DCM-D group exceeded that in the DCM group but remained lower than that in the SHAM group. Notably, a higher level of 8-oxoG DNA expression was observed, suggesting oxidative stress following spinal cord decompression. This model is deemed suitable for analyzing the underlying mechanism of SCII following decompressive cervical laminectomy, as we posit that the obtained results are comparable to the clinical progression of degenerative cervical myelopathy (DCM) post-decompression and exhibit analogous neurological alterations. Notably, this model revealed ischemic reperfusion in the spinal cord after decompression, concomitant with oxidative damage, which plausibly underlies the neurological deterioration observed after decompression.

Plasma 8-Hydroxydeoxyguanosine, 4-Hydroxynonenal and Selenium in Hepatitis B Virus-Infected Adults in Ibadan, Nigeria

Introduction: Hepatitis B Virus (HBV) infection is a significant global health challenge, particularly in Sub-Saharan Africa, including Nigeria. Reactive oxidative species (ROS) generated during HBV replication contribute to redox imbalance, leading to oxidative stress. However, data on the levels of oxidative stress markers in Nigerians infected with HBV is scarce. This study aimed to investigate plasma levels of oxidative stress markers [8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE)] and the trace element, selenium, in HBV-infected adults in Ibadan, Nigeria. Materials and Methods: In a case-control study, 40 HBV-infected patients served as cases, and 40 HBV-uninfected patients served as controls. Anthropometric data were collected, and plasma 8-OHdG and 4-HNE were determined using the ELISA method. Selenium was determined using atomic absorption spectrophotometry. Data were analysed using descriptive, t-test, and Pearson correlation statistics at p = 0.05. Results: The mean ages of HBV-infected and uninfected individuals were 35.3±1.5 and 36.0±1.5 years, respectively. The level of 4-HNE was not significantly different between HBV-infected (2.2±1.7 ng/ml) and uninfected (1.8±1.3 ng/ml). There was also no significant difference in 8-OHdG levels between HBV-infected (4.1±2.4 ng/ml) and uninfected (3.6±1.8 ng/ml). However, in HBV-infected patients, 8-OHdG levels showed a significant positive correlation with 4-HNE (r =0.320, p =0.044). Selenium levels were also significantly higher in HBV-infected (78.4±25.4 ug/dl) than uninfected (35.6±11.4 ug/dl). Conclusion: The levels of markers of lipid peroxidation and DNA oxidation were similar in HBV-infected and uninfected participants, but selenium, the key component of the potent antioxidant glutathione peroxidase was more than double in the infected group. It is plausible that the protective effect of Se may have spared the other markers of oxidative damage. Further studies are needed to elucidate these preliminary findings.

Adjuvant therapy with zinc supplementation; anti-inflammatory and anti-oxidative role in multiple myeloma patients receiving autologous hematopoietic stem cell transplantation: a randomized controlled clinical trial.

Multiple myeloma (MM) patients are often accompanied by heightened levels of oxidative stress, even following bone marrow transplantation. Trace mineral supplements have been found to regulate and inhibit the activity of oxidative radicals and inflammatory factors, which are involved in the pathogenesis of MM. The study sought to evaluate the effectiveness of the supplementation by analyzing changes in oxidative, anti-oxidative, and inflammation markers. Patients were randomly assigned to a zinc or placebo group, with the former receiving 30mg of zinc or placebo tablets daily for 1month. Blood samples were collected from the patients on the day of transplantation, 15days, and 30days post-transplantation. Real-time PCR was employed to measure the expression of oxidative/antioxidative genes. Furthermore, the protein level of oxidative markers in serum samples was assessed. Finally, serum TNF-α concentrations were measured using the ELISA technique. The expression levels of SOD1, SOD2, and NRF2 genes were significantly higher on days 15 and 30 compared to the control group (P < 0.05), with a greater increase on day 30 (P < 0.05). Conversely, the expression levels of Keap1 and NOX2 genes were lower on day 30 than those of the control group (P < 0.05), with a further decrease from day 15 to day 30 (P < 0.05). The experimental group exhibited a notable reduction in TNF-α cytokine levels on day 30 compared to the control and placebo groups (P < 0.05). All findings were coordinated according to the nutritional questionnaire. Our findings suggest a potential benefit of zinc supplementation in managing the adverse effects of chemotherapy in MM patients, warranting further investigation.

Effects of β-sitosterol on anxiety in migraine-induced rats: The role of oxidative/nitrosative stress and mitochondrial function.

Anxiety often coexists with migraine, and both conditions share a commonality in oxidative/nitrosative stress and mitochondrial dysfunction contributing to their pathogenesis. β-Sitosterol, a plant sterol, has shown promise in mitigating oxidative/nitrosative stress, enhancing mitochondrial function, and exerting neuroprotective effects. In this study, we investigated the impact of β-sitosterol on migraine-associated anxiety and whether this effect was associated with alleviation of oxidative/nitrosative stress and improvement in mitochondrial function. Nitroglycerin was used to induce migraine in adult male Wistar rats. β-Sitosterol treatment consisted of daily intraperitoneal injections (10 mg/kg) for 10 days following migraine induction. Anxiety levels were evaluated using open-field test (OFT) and hole-board test (HBT). Frontal cortex samples were analyzed for malondialdehyde (MDA), glutathione (GSH), reactive oxygen/nitrogen species, nitric oxide (NO) (markers of oxidative/nitrosative stress), and ATP (indicator of mitochondrial function). Migraine induction led to impaired performance in both the OFT and the HBT. Concurrently, it elevated MDA, reactive oxygen/nitrogen species, and NO levels while diminishing GSH levels in the frontal cortex, signifying heightened oxidative/nitrosative stress. Moreover, ATP levels decreased, indicating mitochondrial dysfunction. Treatment with β-sitosterol significantly restored performance in both behavioral assays and normalized the levels of MDA, GSH, reactive oxygen/nitrogen species, NO, and ATP. β-Sitosterol exerted anxiolytic effects in migraine, which can be attributed to its ability to ameliorate oxidative/nitrosative stress and enhance mitochondrial function.

Impact of Age on some Oxidant and Antioxidants Marker During Menstrual Cycles

Impact of Age on some Oxidant and Antioxidants Marker During Menstrual Cycles

Effect of Mobile Phone Base Stations on Antioxidant and Oxidant Serum Levels: Possible Impact on Cancer Development

Background: There have been claims of a potential link between radio frequency (RF) emissions from mobile phone stations and cancer. In addition, widespread public concern has been expressed about the placement of cell phone antennas due to concerns about the risk of cancer. Objective: The objective of the study was to assess the effect of mobile phone base stations on oxidant and antioxidant markers and to investigate its potential correlation with cancer progression. Methods: The study involved three groups: cancer patients, healthy individuals residing near mobile phone base stations, and a control group living away from such base stations. Results: The study revealed significant differences in most biochemical parameters among the groups, highlighting the impact of mobile phone base stations on health. Cancer patients residing near mobile phone base stations (Group 1) showed notable changes compared to healthy individuals living both near (Group 2) and far (Group 3, control group) from mobile phone base stations. Specifically, the harmful effects of mobile phone base stations were evident in the increased total oxidant status (TOS), decreased total antioxidant capacity (T-AOC), and altered liver enzymatic activities (AST, ALP, ALT, LDH). Conclusion: This study finding suggests that proximity to mobile phone base stations may negatively influence oxidative stress and liver function leading to cancer. Further research is necessary to fully understand these effects and develop appropriate public health strategies.

Ameliorative effect of α-tocopherol and curcumin against the deleterious effects of hydrogenated (thermally oxidized) rice bran oil in rats

Rice bran oil (RBO) is known for its health benefits due to its high content of natural antioxidants like tocotrienols, tocopherols, and oryzanols, which combat oxidative stress and inflammation. However, repeated heating of RBO above 110°C leads to degradation, forming harmful oxidative components and reducing its antioxidant content. This study aimed to investigate the effects of long-term consumption of thermally oxidized RBO on rats and the potential protective effects of curcumin and α-tocopherol supplementation. RBO was subjected to oxidative degradation through repeated frying cycles at temperatures ranging from 100°C to 180°C for 45 days. Physicochemical and phytochemical parameters of the oxidized RBO were analyzed. In vivo experiments evaluated serum biochemical, hematological, and histopathological parameters, along with oxidative and inflammatory responses in rats fed with oxidized RBO for 45 days. Results showed that thermal oxidation at 180°C significantly altered the chemical composition of RBO, increasing oxidative markers and reducing nutritional components. Consumption of oxidized RBO led to decreased body weight gain, elevated levels of various biochemical markers indicating liver and kidney dysfunction, hyperlipidemia, and increased oxidative and inflammatory damage in rats. However, supplementation with curcumin and α-tocopherol effectively mitigated these harmful effects. In conclusion, long-term consumption of thermally oxidized RBO negatively affects health parameters in rats, but fortification with curcumin and α-tocopherol helps alleviate these adverse effects

Effect of Levetiracetam on Oxidant-Antioxidant Activity during Long-Term Temporal Lobe Epilepsy in Rats.

Epilepsy is a disorder characterized by a predisposition to generate seizures. Levetiracetam (LEV) is an antiseizure drug that has demonstrated oxidant-antioxidant effects during the early stages of epilepsy in several animal models. However, the effect of LEV on oxidant-antioxidant activity during long-term epilepsy has not been studied. Therefore, the objective of the present study was to determine the effects of LEV on the concentrations of five antioxidant enzymes and on the levels of four oxidant stress markers in the hippocampus of rats with temporal lobe epilepsy at 5.7 months after status epilepticus (SE). The results revealed that superoxide dismutase (SOD) activity was significantly greater in the epileptic group (EPI) than in the control (CTRL), CTRL + LEV and EPI + LEV groups. No significant differences were found among the groups' oxidant markers. However, the ratios of SOD/hydrogen peroxide (H2O2), SOD/glutathione peroxidase (GPx) and SOD/GPx + catalase (CAT) were greater in the EPI group than in the CTRL and EPI + LEV groups. Additionally, there was a positive correlation between SOD activity and GPx activity in the EPI + LEV group. LEV-mediated modulation of the antioxidant system appears to be time dependent; at 5.7 months after SE, the role of LEV may be as a stabilizer of the redox state.