Search Results (1,711)

Brain ischemia-reperfusion (I/R) injury, commonly occurring in ischemic stroke and post-cardiac arrest scenarios, results in complex secondary damage involving oxidative stress, inflammation, apoptosis, and blood-brain barrier (BBB) breakdown. Despite decades of research, no pharmacological agent has yet been clinically approved for post-I/R neuroprotection. Natural compounds have recently gained attention for their multimodal therapeutic potential, including antioxidant, anti-inflammatory, anti-apoptotic, and neuroregenerative effects. This review highlights nine promising candidates—resveratrol, curcumin, quercetin, berberine, ginkgolide B, baicalin, naringin, fucoidan, and astaxanthin—that exhibit efficacy in experimental models of I/R injury when administered after the insult. Their chemical structures, pharmacokinetics, and mechanisms of action are described in detail, focusing on key signaling pathways such as nuclear factor erythroid 2-related (Nrf2), nuclear factor kappa B (NF-κB), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), and brain-derived neurotrophic factor (BDNF). Importantly, we outline the selection criteria for these compounds, including demonstrated neuroprotective efficacy, mechanistic clarity, and translational feasibility. While several challenges remain—such as limited bioavailability, BBB penetration, and species-specific metabolism—emerging strategies like nanoparticle delivery, synthetic analogs, and drug combinations offer potential solutions. By emphasizing the therapeutic versatility and mechanistic diversity of these natural agents, this review supports their clinical potential and encourages further preclinical optimization and biomarker-guided human trials. Full article

Facial bone fractures represent a significant clinical challenge due to their impact on function, aesthetics, and quality of life. Despite advances in imaging and surgical techniques, early and accurate assessment of the healing process remains limited. Conventional diagnostic methods often detect complications, such as delayed union or non-union, too late for optimal intervention. Oxidative stress—an imbalance between reactive oxygen species (ROS) and antioxidant defenses—plays a critical role in bone regeneration. In this review, biomarkers are presented in two main categories: (1) oxidative damage biomarkers (lipid peroxidation products: malondialdehyde, 4-hydroxynonenal, and F2-isoprostanes) and (2) antioxidant biomarkers (glutathione, enzymatic antioxidants: SOD, GPx, CAT). Their potential as non-invasive diagnostic and prognostic tools in craniofacial fracture healing is evaluated, along with emerging therapeutic strategies. Monitoring their levels in blood samples may provide real-time insights into the dynamics of fracture repair, enabling earlier detection of healing disturbances and informing personalized treatment approaches. Full article

Background: Oxidative stress (OS) and inflammation are interconnected processes with significant roles in various chronic diseases, particularly those associated with aging, such as metabolic syndrome (MetS). Recent evidence suggests that walnuts (from Juglans regia L.), due to their rich content of phytochemicals, have antiaging potential by attenuating OS and chronic low-grade inflammation, known as inflammaging. Objectives: We aimed to assess the impact of daily walnut consumption for 4 weeks on biomarkers of OS and inflammation in a cohort of middle-aged individuals at risk of developing MetS. Methods: In this crossover randomized controlled trial (RCT), 22 participants (mean age: 48.81 ± 4.3 years) underwent two 28-day dietary interventions separated by a one-month washout period. One intervention period included daily consumption of 45 g of walnuts, while the other (control period) involved a normal-calorie diet without walnuts. Catalase (CAT) and glutathione peroxidase (GPx) activities, total antioxidant capacity (TAC), and interleukin (IL-1β, IL-6, IL-8) and tumor necrosis factor alpha (TNF-α) levels were determined from serum before and after each intervention period. Results: Assessment of changes obtained for the selected biomarkers following the walnut and control-diet periods (final-baseline) showed slight changes, but without any statistical significance, among the 20 participants included in the analysis. Conclusions: This first RCT targeting a group of middle-aged adults at risk of developing MetS shows that short-term (4 weeks) daily walnut consumption did not significantly alter oxidative stress and inflammation parameters, thus potentially contributing to the maintenance of cellular homeostasis. Further research is needed to investigate the impact of daily walnut consumption over a longer period (>3 months) on oxidative and inflammatory status in the middle-aged population and its potential to positively impact MetS biomarkers. Full article

Background and Objectives: Obstructive sleep apnea (OSA) represents an increasing public health concern, closely linked with cardiovascular, metabolic, and neurocognitive disorders, as well as impaired quality of life. The complex pathophysiology of OSA involves upper airway dysfunction, oxidative stress, and inflammation, with endothelial dysfunction considered central to its associated comorbidities. Despite notable advances in OSA research, the biological mechanisms driving these complications remain insufficiently understood. The present study aimed to examine the associations between redox status, proinflammatory biomarkers, and the gene expression of full-length receptor for advanced glycation end products (flRAGE) and transforming growth factor beta 1 (TGF-β1) in relation to the presence and severity of OSA. Materials and Methods: The study cohort comprised 125 participants with diagnosed OSA and 42 controls without evidence of OSA. General and clinical characteristics were recorded for all participants. Laboratory analyses included the assessment of redox and inflammatory markers in serum and plasma, while flRAGE and TGF-β1 messenger ribonucleic acids (mRNA) were quantified in peripheral blood mononuclear cells. Results: Patients with OSA demonstrated elevated oxidative stress and inflammation, characterized by increased total antioxidant status (TAS) and C-reactive protein CRP levels, together with reduced concentrations of soluble RAGE (sRAGE). The severity of OSA, indicated by the apnea-hypopnea index, increases total oxidative status (TOS) and TGF-β1 mRNA, while sRAGE decreases. The sRAGE–ROS-related factor was negatively associated with OSA, whereas the redox status factor showed a positive association. TOS was independently and positively correlated with OSA severity. Conclusions: Individuals with OSA exhibit a state of enhanced oxidative stress and inflammation. Increasing severity of OSA was associated with rising TOS and TGF-β1 mRNA expression, accompanied by declining sRAGE concentrations. A combined redox–inflammatory biomarker profile was found to be associated with both the presence and severity of OSA. Full article

Objectives: This study aimed to evaluate marjoram’s ameliorative effects in a letrozole-induced PCOS rat model and to explore its mechanism of action, focusing on Nrf2 activation and NF-κB suppression in ovarian tissue. Methods: In this study, PCOS was induced by the oral administration of letrozole (1 mg/kg/day) for 21 days. Rats were then divided into six groups: control (0.5% CMC), letrozole, letrozole + metformin (2 mg/100 g), and letrozole + MRJ extract (20, 40, or 60 mg/kg). All groups received oral treatment for 21 days. Biochemical analysis was performed using serum and plasma; while ovarian tissue homogenate was used for antioxidant enzymes and inflammatory and apoptosis biomarkers. Results: The letrozole-treated animals exhibited significant increases in final body weights, as well as ovary length and weight. In terms of biochemical parameters, there were significant increases in fasting blood glucose and insulin, HOMA-IR, and serum levels of cholesterol, triglycerides (TGs), and LDL-c and a decrease in HDL levels. Concerning the hormonal profile, testosterone and LH levels were significantly elevated while a notable decrease in FSH and estradiol levels was observed. Similarly, letrozole-treated rats showed significantly elevated levels of MDA and many other inflammatory mediators such as IL-6, TNF-α, and ICAM-1. A significant increase in the markers of intrinsic cell apoptosis, such as Bax and caspase-3, and the reduced levels of Bcl-2 and antioxidant mediators, including GSH, SOD, and HO-1, as well as mRNA and nuclear expression of Nrf2, compared to control rats, have been reported. The ovaries of the rats with PCOS treated with metformin and MRJ (60 mg/kg) showed the most significant improvements. Similarly, TEM also demonstrated a dose-dependent ameliorating effect. Conclusions: The current study highlights marjoram’s protective effect against letrozole-induced ovarian damage in rats with polycystic ovarian syndrome, suggesting its potential as a complementary and therapeutic agent for managing PCOS. Full article

Oxidative stress plays a key role in tissue damage during inflammation, highlighting the need for effective antioxidant interventions. This study investigates the antioxidant potential of argan oil (AO)—obtained from Argania spinosa (L.) Skeels almonds—in comparison with olive oil (OO), cactus seed oil (CSO), and colza oil (CO). Quantitative analyses of total polyphenols and pigments—including chlorophylls, carotenoids, and xanthophylls—were conducted alongside antioxidant capacity assessments via DPPH, ABTS, and FRAP assays. The methanolic fraction consistently demonstrated the highest phenolic concentration and antioxidant efficacy across all oils. To establish in vivo relevance, a male C57BL/6J mouse model of acute oxidative stress was induced by lipopolysaccharide (LPS) administration. Pretreatment with oils significantly modulated key oxidative stress biomarkers—SOD, CAT, GPx activities, GSH levels, and lipid peroxidation (MDA)—in both heart and kidney. LPS challenge induced marked oxidative imbalance, notably increasing enzymatic activity and MDA levels, while depleting GSH in the heart and elevating it in the kidney. However, pretreatment with oils effectively restored redox homeostasis, with AO showing particularly potent effects and a stronger regulatory effect observed in the kidney. Hierarchical clustering of z-score-normalized heatmaps revealed distinct oxidative stress signatures, clearly separating LPS-treated heart and kidney tissues from other groups due to heightened oxidative markers. In contrast, oil-treated and oil-combined-with-LPS groups clustered closer to the control, underscoring the protective effect of oils against LPS-induced oxidative stress, with efficiency varying by oil type. Pearson correlation analysis, complemented by multivariate principal component analysis (PCA), further emphasized strong positive associations between antioxidant enzymes (SOD, CAT, GPx) and MDA levels, while GSH exhibited tissue-specific behavior—negatively correlated in the heart but positively in the kidney—highlighting divergent redox regulation between organs. Collectively, AO demonstrated robust cardioprotective and nephroprotective properties, supporting its potential as a natural dietary strategy against inflammation-induced oxidative stress. Full article

Psychiatric disorders such as major depressive disorder, bipolar disorder, and schizophrenia are now recognized as complex systemic conditions in which mitochondrial dysfunction and oxidative stress are key contributors to their pathophysiology. Mitochondria, beyond their role in ATP synthesis, are critical for calcium regulation, immune responses, and apoptosis, and their impairment affects brain function. This review examines current evidence from transcriptomics, metabolomics, neuroimaging, and preclinical studies, which consistently show disruptions in oxidative phosphorylation, mitochondrial fragmentation, altered mitochondrial DNA, and heightened inflammatory activity across these disorders. We integrate recent advances with the understanding of mitochondrial bioenergetics in the brain, the contribution of redox imbalance to neural dysfunction, the crosstalk between mitochondria and immune mechanisms, and the relevance of these processes to clinical symptoms. Furthermore, we highlight the promise of bioenergetic biomarkers and emerging interventions targeting mitochondrial pathways, including antioxidants, AMPK-SIRT1-PGC-1α axis modulators, physical exercise, and mitoprotective agents. Peripheral metabolic signatures and neuroimaging modalities are also discussed as tools for diagnostic refinement and individualized therapeutic approaches. These insights underscore the centrality of mitochondrial health in psychiatric disease and support the development of precision psychiatry grounded in metabolic phenotyping. Full article

During pregnancy, uterine circulation undergoes profound structural and functional adaptations to accommodate the dramatically increased metabolic demands of the growing fetus. Oxidative stress (OS) and inflammation have emerged as central regulators both physiologically, to drive vascular remodeling and angiogenesis, and pathologically, when dysregulated, to promote endothelial dysfunction, maladaptive extracellular matrix (ECM) remodeling, and heightened arterial stiffness. This review synthesizes insights into the molecular sources of reactive oxygen species (ROS) in the uterine vasculature, endothelial and immune-mediated inflammatory pathways, the bidirectional crosstalk between OS and inflammation, and their combined impact on vascular stiffness. We further discuss clinical implications for conditions such as preeclampsia and intrauterine growth restriction (IUGR), highlight circulating and imaging biomarkers of redox–inflammatory imbalance, and evaluate antioxidant and anti-inflammatory therapeutic strategies. Finally, we identify critical knowledge gaps and propose future research directions aimed at translating mechanistic understanding into personalized maternal–fetal care. For this narrative review, we searched the PubMed and Web of Science databases to identify all human and animal studies investigating OS and inflammation on uterine vasculature remodeling during pregnancy. Full article

Oxidative stress, defined as the imbalance between reactive oxygen species (ROS) and antioxidant defenses, plays a pivotal role in the pathogenesis of several pregnancy complications, notably preeclampsia (PE), gestational diabetes mellitus (GDM), fetal growth restriction (FGR), and recurrent pregnancy loss (RPL). During normal pregnancy, low to moderate ROS levels support essential placental functions such as angiogenesis and trophoblast differentiation. However, excessive ROS production overwhelms antioxidant systems, leading to lipid peroxidation, protein and DNA damage, and impaired placental function. This review synthesizes current evidence linking oxidative stress to adverse pregnancy outcomes, highlighting key biomarkers such as malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and 8-iso-prostaglandin F2α (8-iso-PGF2α). While antioxidant therapies—particularly vitamins C and E, selenium, and folic acid—have shown promise in reducing oxidative markers, their impact on clinical outcomes remains inconsistent. The variability in results underscores the need for standardized biomarker protocols and personalized treatment strategies based on genetic predispositions and baseline oxidative status. Future research may better harness antioxidant interventions to improve maternal–fetal health by addressing these gaps. Full article

Menopause is a natural and inevitable part of life for women, leading to many physical and psychological changes accompanied by declining estrogen levels. This systematic review aimed to evaluate the effect of curcumin, due to its antioxidant and anti-inflammatory properties, on postmenopausal outcomes in women. This comprehensive analysis of RCTs (randomized controlled trials) published in the last decade was selected through a search of PubMed, Wiley, Scopus, and Web of Science (PROSPERO Identifier: CRD42024549735). Study selection and data extraction were performed using exclusion and inclusion criteria according to the PICOS framework (P: Population, I: Intervention, C: Comparison, O: Outcomes, S: Study designs). Of the twelve studies that met the criteria, 11 had a low-risk bias, but reports were conflicting on serum estradiol levels, bone density markers, and vasomotor symptoms; no significant effects on physical, psychological, or sexual functions were observed. For cardiometabolic biomarkers, short-term curcumin intake showed no significant effects, while long-term interventions using bioavailable forms of curcumin showed improvements in serum fasting glucose, fasting insulin, HOMA-IR (Homeostatic Model Assessment of Insulin Resistance), and lipid parameters. There are a limited number of studies examining the effect of curcumin intake on menopause-related outcomes. While overdose has been observed in some studies attempting to restore estradiol levels, no significant effects have been observed. However, curcumin intake impacts postmenopausal symptoms (e.g., improving symptoms of osteoporosis) through its antioxidant and anti-inflammatory effects. Different forms and doses, combinations, and durations of interventions may influence outcomes. Better-designed studies are needed to understand the potential effects of curcumin intake during menopause. Full article

Neurodegenerative diseases such as Alzheimer’s disease (AD) are closely linked to oxidative stress and advanced glycation end products (AGEs), two interrelated processes that exacerbate neuronal damage through mitochondrial dysfunction, protein aggregation, and chronic inflammation. This narrative review explores the metabolic interplay between reactive oxygen species (ROS) and AGEs, with a focus on the AGE-RAGE (receptor for advanced glycation end products) signaling axis as a driver of neurodegeneration. Evidence from preclinical and clinical studies highlights their combined role in disease progression and underscores potential therapeutic targets. Strategies including mitochondria-targeted antioxidants, AGE inhibitors, RAGE antagonists, and metabolic interventions are discussed, along with future directions for biomarker development and personalized treatments. This review integrates current molecular insights into a unified metabolic–inflammatory model of AD, highlighting translational therapeutic opportunities. Full article

Rheumatoid arthritis (RA) is one of the most common chronic autoimmune diseases which global prevalence is approximately 0.3–2%. Numerous studies provide evidence that the elevated levels of reactive oxygen species (ROS) contribute to the pathogenesis and progression of RA. In response to redox imbalance, several intrinsic antioxidant defence mechanisms are activated to counteract oxidative stress and scavenge ROS. The aim of the present study is to analyse whether the levels of lactoferrin and thioredoxin, two proteins which are part of the antioxidant defence of the body, are associated with fibrinogen and other acute phase proteins such as CRP and ferritin in RA. Serum lactoferrin, thioredoxin, ferritin, and CRP levels were measured using ELISA. Significant positive correlations of lactoferrin and thioredoxin with fibrinogen were observed in RA patients, r = 0.394, p < 0.0001 and r = 0.410, p = 0.002, respectively. These positive correlations were also observed in females, r = 0.375, p < 0.0001 and r = 0.447, p = 0.001, in the subgroup of patients with DAS28 < 5.1, r = 0.689, p < 0.0001 and r = 0.604, p = 0.001 and in the subgroup of patients with normal CRP, r = 0.488, p < 0.0001 and r = 0.414, p = 0.005, respectively. These findings help clarify the pathogenetic interplay between oxidative stress, inflammation, and coagulation in RA and indicate the need for further studies to elucidate the potential of lactoferrin and thioredoxin as biomarkers that capture pathological disease changes. Full article

This review aims to provide a comprehensive overview of how oxidative stress drives inflammation, structural remodeling, and clinical expression of childhood asthma, while critically appraising emerging redox-sensitive biomarkers and antioxidant-focused preventive and therapeutic strategies. Oxidative stress arises when reactive oxygen species (ROS) and reactive nitrogen species (RNS) outpace airway defenses. This surplus provokes airway inflammation: ROS/RNS activate nuclear factor kappa-B (NF-κB) and activator protein-1 (AP-1), recruit eosinophils and neutrophils, and amplify type-2 cytokines. Normally, an antioxidant network—glutathione (GSH), enzymes such as catalase (CAT) and superoxide dismutase (SOD), and nuclear factor erythroid 2-related factor 2 (Nrf2)—maintains redox balance. Prenatal and early exposure to fine particulate matter <2.5 micrometers (µm) (PM_2.5), aeroallergens, and tobacco smoke, together with polymorphisms in glutathione S-transferase P1 (GSTP1) and CAT, overwhelm these defenses, driving epithelial damage, airway remodeling, and corticosteroid resistance—the core of childhood asthma pathogenesis. Clinically, biomarkers such as exhaled 8-isoprostane, hydrogen peroxide (H₂O₂), and fractional exhaled nitric oxide (FeNO) surge during exacerbations and predict relapses. Therapeutic avenues include Mediterranean-style diet, regular aerobic exercise, pharmacological Nrf2 activators, GSH precursors, and mitochondria-targeted antioxidants; early trials report improved lung function and fewer attacks. Ongoing translational research remains imperative to substantiate these approaches and to enable the personalization of therapy through individual redox status and genetic susceptibility, ultimately transforming the care and prognosis of pediatric asthma. Full article

Carbon dots (CDs) are gaining significant attention as multifunctional nanomaterials due to their optical properties, aqueous dispersibility, redox activity, and overall biocompatibility. This review presents a critical overview of the recent advances concerning the application of CDs in nucleic acid-centered diagnostics, with a specific focus on oxidative DNA damage. The use of CDs for the detection of oxidative DNA damage biomarkers, such as 8-oxo-2′-deoxyguanosine (8-oxo-dG), and their potential roles as fluorescent probes in environments related to oxidative stress is discussed in detail. The relationship between surface functionalization and biological performance is examined, highlighting how physicochemical properties dictate both the beneficial and adverse biological responses to CDs. Remarkably, CDs can act as antioxidants, mitigating oxidative damage, or as pro-oxidants, inducing cytotoxic effects, an ambivalent behavior that can be strategically harnessed for cytoprotection or selective tumor cell killing. Overall, this review outlines how CDs can contribute to the development of precision tools for studying oxidative environments affecting nucleic acids, with important implications for both diagnostics and redox-based therapeutic strategies of human diseases. Full article

Despite their crucial biological role as metabolites, reactive oxygen and reactive nitrogen species (ROS and RNS) can have a negative effect on organisms when their cellular contents overwhelm the normal equilibrium provided by antioxidant defenses. Important biomolecules, such as lipids, proteins, and nucleic acids (i.e., DNA), can be damaged by their oxidative effects, resulting in malfunction or a shorter lifespan of cells and, eventually, of the whole organism. Oxidative stress can be defined as the consequence of an imbalance of pro-oxidants and antioxidants due to external stress sources (e.g., exposure to xenobiotics, UV radiation, or thermic stress). It can be evaluated by monitoring specific biomarkers to determine the state of health of breathing organisms. Assessments of ROS, RNS, specific degenerative oxidative reaction products, and antioxidant system efficiency (antioxidant enzyme activities and antioxidant compound contents) have been extensively performed for this purpose. A wide variety of analytical methods for measuring these biomarkers exist in the literature; most of these methods involve indirect determination via spectrophotometric and spectrofluorometric techniques. This review reports a collection of studies from the last decade regarding contaminant-induced oxidative stress in insects, with a brief description of the analytical methods utilized. Full article