Search Results (392)

Background/Objectives: Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide, driven largely by underlying coronary artery disease (CAD). Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play pivotal mechanistic roles in endothelial dysfunction, atherosclerotic plaque progression, and subsequent cardiac injury. Excessive production of these reactive species disrupts cellular redox balance, promotes mitochondrial dysfunction, and accelerates vascular inflammation, ultimately contributing to plaque rupture and MI. This study aimed to investigate the mechanistic associations and clinical correlations of individual ROS and RNS markers in patients with MI. Methods: We conducted a case–control study including 86 patients with MI and 60 age- and sex-matched controls without cardiovascular disease, recruited from the Medina Cardiac Center in Saudi Arabia. The MI cohort was subdivided into ST-elevation MI (STEMI, n = 62) and non-ST-elevation MI (NSTEMI, n = 24) to explore potential differences in oxidative and nitrosative stress profiles. Serum levels of multiple ROS (including hydrogen peroxide, hydroxyl radical, and superoxide anion) and RNS (including nitric oxide and peroxynitrite) were quantified using validated fluorescence-based assays. Clinical and biochemical parameters, including lipid profiles, troponin, and left ventricular ejection fraction, were also assessed. Results: Most ROS and RNS markers were significantly elevated in MI patients compared to controls (p < 0.05), except for nitrogen dioxide. Moderate to strong positive correlations were observed between ROS/RNS levels and serum total cholesterol and LDL-cholesterol (p < 0.001). In contrast, weak or non-significant correlations were found between ROS/RNS markers and serum troponin or left ventricular ejection fraction. Both STEMI and NSTEMI subgroups demonstrated significantly higher oxidative and nitrosative stress levels compared to controls, with distinct patterns between the subtypes. Conclusions: This study underscores a mechanistic link between elevated ROS/RNS levels and myocardial infarction, supporting the importance of targeting oxidative and nitrosative pathways as potential therapeutic strategies. 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

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

The use of a wide variety of antioxidants has been advocated as a means to prevent, delay the progression of, or counteract the adverse consequences of sarcopenia, such as loss of muscle strength, muscle quantity/quality, and physical performance. However, these proposals do not always appear to be supported in the literature by a thorough understanding of the contribution of redox perturbations to the pathogenesis of sarcopenia, nor of the biochemical properties, mechanism of action, pharmacokinetics, and pharmacodynamics of different antioxidants. This review discusses these aspects, aiming to provide a rationale for the selection and use of antioxidants in sarcopenia. After providing a definition of sarcopenia in the context of frailty, we distinguish between oxidative eustress as a physiological response of muscle cells to mild stimulation, such as moderate exercise, mediating their capacity for adaptation and regeneration, and oxidative distress as a pathophysiological response to muscle cell damage and death. The role of oxidative damage to biological macromolecules, both direct and mediated by advanced lipid peroxidation end products and advanced glycation/glycoxidation end products, is examined in detail. Next, we discuss antioxidant defense mechanisms, both enzymatic and non-enzymatic, including redox-sensitive gene regulatory events presided over by nuclear factor erythroid 2-related factor 2, the master regulator of enzymatic antioxidants. The review then discusses criteria for a rational classification of non-enzymatic antioxidants. This is followed by a review of some of the main radical-trapping antioxidants, both phenolic and non-phenolic, whose characteristics are compared. Full article

Skin aging is a complex biological process influenced by intrinsic factorssuch as genetic predispositions and hormonal changes as well as extrinsic factors including ultraviolet radiation, environmental pollution, and lifestyle habits. This process culminates in a progressive decline in the structural and functional integrity of the skin. This review delves into the protective roles of carotenoids, highlighting their significant anti-oxidative, anti-inflammatory, and photoprotective properties. We included studies that investigated the effects of dietary or topical carotenoids on skin aging markers in human and animal models. Eligible studies were identified through searches of PubMed, Scopus, Web of Science, Embase, Google Scholar, and the Cochrane Library from January 2000 to March 2025. Risk of bias was assessed using the Cochrane RoB tool for randomized trials and animal studies. A total of 176 studies were included, and data were synthesized narratively due to heterogeneity in study designs and outcomes. The findings indicate that carotenoids mitigate oxidative stress-induced cellular damage by scavenging reactive oxygen species (ROS) and Reactive Nitrogen Species (RNS), attenuating chronic inflammation, and enhancing dermal matrix integrity via collagen biosynthesis and modulation of matrix metalloproteinases. Additionally, they support skin hydration and elasticity by indirectly regulating aquaporins and promoting hyaluronic acid synthesis. This review further explores emerging strategies that incorporate carotenoid supplementation in lifestyle medicine and preventive dermatology. By elucidating the cellular pathways through which carotenoids exert their effects and modulate mitochondrial function, this review highlights their translational potential in anti-aging skincare. Ongoing research is essential to comprehend the complex connections between carotenoids, skin physiology, and overall health. This understanding will ultimately facilitate the creation of personalized nutritional and dermocosmetic strategies. Full article

Oxidative stress is a defining and pervasive driver of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). As a molecular accelerant, reactive oxygen species (ROS) and reactive nitrogen species (RNS) compromise mitochondrial function, amplify lipid peroxidation, induce protein misfolding, and promote chronic neuroinflammation, creating a positive feedback loop of neuronal damage and cognitive decline. Despite its centrality in promoting disease progression, attempts to neutralize oxidative stress with monotherapeutic antioxidants have largely failed owing to the multifactorial redox imbalance affecting each patient and their corresponding variation. We are now at the threshold of precision redox medicine, driven by advances in syndromic multi-omics integration, Artificial Intelligence biomarker identification, and the precision of patient-specific therapeutic interventions. This paper will aim to reveal a mechanistically deep assessment of oxidative stress and its contribution to diseases of neurodegeneration, with an emphasis on oxidatively modified proteins (e.g., carbonylated tau, nitrated α-synuclein), lipid peroxidation biomarkers (F2-isoprostanes, 4-HNE), and DNA damage (8-OHdG) as significant biomarkers of disease progression. We will critically examine the majority of clinical trial studies investigating mitochondria-targeted antioxidants (e.g., MitoQ, SS-31), Nrf2 activators (e.g., dimethyl fumarate, sulforaphane), and epigenetic reprogramming schemes aiming to re-establish antioxidant defenses and repair redox damage at the molecular level of biology. Emerging solutions that involve nanoparticles (e.g., antioxidant delivery systems) and CRISPR (e.g., correction of mutations in SOD1 and GPx1) have the potential to transform therapeutic approaches to treatment for these diseases by cutting the time required to realize meaningful impacts and meaningful treatment. This paper will argue that with the connection between molecular biology and progress in clinical hyperbole, dynamic multi-targeted interventions will define the treatment of neurodegenerative diseases in the transition from disease amelioration to disease modification or perhaps reversal. With these innovations at our doorstep, the future offers remarkable possibilities in translating network-based biomarker discovery, AI-powered patient stratification, and adaptive combination therapies into individualized/long-lasting neuroprotection. The question is no longer if we will neutralize oxidative stress; it is how likely we will achieve success in the new frontier of neurodegenerative disease therapies. Full article

Plants are constantly exposed to environmental stressors such as drought, salinity, and extreme temperatures, which threaten their growth and productivity. To counter these challenges, they employ complex molecular defense systems, including epigenetic modifications that regulate gene expression without altering the underlying DNA sequence. This review comprehensively examines the emerging roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) as central signaling molecules orchestrating epigenetic changes in response to abiotic stress. In addition, biotic factors such as pathogen infection and microbial interactions are considered for their ability to trigger ROS/RNS generation and epigenetic remodeling. It explores how ROS and RNS influence DNA methylation, histone modifications, and small RNA pathways, thereby modulating chromatin structure and stress-responsive gene expression. Mechanistic insights into redox-mediated regulation of DNA methyltransferases, histone acetyltransferases, and microRNA expression are discussed in the context of plant stress resilience. The review also highlights cutting-edge epigenomic technologies such as whole-genome bisulfite sequencing (WGBS), chromatin immunoprecipitation sequencing (ChIP-seq), and small RNA sequencing, which are enabling precise mapping of stress-induced epigenetic landscapes. By integrating redox biology with epigenetics, this work provides a novel framework for engineering climate-resilient crops through the targeted manipulation of stress-responsive epigenomic signatures. Full article

The accelerated increase in atmospheric CO₂ concentration is one of the most pressing problems at present. It is possible that this increase causes slight modifications in intracellular CO₂. The aim of this work was to determine whether CO₂ at different concentrations can affect the oxidative damage caused by ciprofloxacin (CIP) in Escherichia coli and to evaluate the possible implications of this effect for human health. To identify the effects of CO₂ on the action of CIP, reactive oxygen (ROS) and reactive nitrogen (RNS) species were measured at two different CO₂ concentrations while monitoring the bacterial antioxidant response. These assays showed that CO₂ led to a decrease in ROS formation relative to that under atmospheric conditions (ACs), while it had the opposite effect on RNS formation, which increased relative to that under ACs. Under CO₂ conditions, antioxidant defenses were less activated, with superoxide dismutase, catalase, and ferric reducing assay potency decreasing compared to those under ACs; however, reduced glutathione exhibited the opposite behavior. In the presence of CO₂, the activity of CIP against E. coli was reduced relative to that under ACs. In conclusion, CO₂ interferes with the action of CIP in bacterial cells, generating changes in oxidative stress. Full article

As two pivotal regulatory factors in cancer biology, oxidative stress and inflammation interact dynamically through complex network mechanisms to influence tumor initiation, progression, and treatment resistance. Oxidative stress induces genomic instability, oncogenic signaling activation, and tumor microenvironment (TME) remodeling via the abnormal accumulation of reactive oxygen species (ROS) or reactive nitrogen species (RNS). Conversely, inflammation sustains malignant phenotypes by releasing pro-inflammatory cytokines and chemokines and promoting immune cell infiltration. These processes create a vicious cycle via positive feedback loops whereby oxidative stress initiates inflammatory signaling, while the inflammatory milieu further amplifies ROS/RNS production, collectively promoting proliferation, migration, angiogenesis, drug resistance, and immune evasion in tumor cells. Moreover, their crosstalk modulates DNA damage repair, metabolic reprogramming, and drug efflux pump activity, significantly impacting the sensitivity of cancer cells to chemotherapy, radiotherapy, and targeted therapies. This review systematically discusses these advances and the molecular mechanisms underlying the interplay between oxidative stress and inflammation in cancer biology. It also explores their potential as diagnostic biomarkers and prognostic indicators and highlights novel therapeutic strategies targeting the oxidative stress–inflammation axis. The goal is to provide a theoretical framework and translational roadmap for developing synergistic anti-tumor therapies. Full article

Perfluorooctanoic acid (PFOA) and its short-chain substitutes, perfluorohexanoic acid (PFHxA) and perfluorobutanoic acid (PFBA), are persistent environmental pollutants associated with widespread human exposure through occupational and environmental routes. The aim of this was to investigate the effects of PFOA, PFHxA, and PFBA on the intracellular level of adenosine-5’-triphosphate (ATP) in human peripheral blood mononuclear cells (PBMCs) and their viability, size, and granularity. Moreover, oxidative and nitrosative stress was assessed based on the levels of reactive oxygen species (ROS), reactive nitrogen species (RNS), and highly reactive oxygen species (hROS, mainly hydroxyl radical). Finally, oxidative damage to protein and lipids in PBMCs was measured. The cells were incubated for 1 h and 24 h at concentrations correlated to human occupational and environmental exposure (0.001–200 µg/mL) to the substances. Our findings indicate that PFOA and its short-chain analogs cause different effects in human PBMCs. PFOA induced statistically significant alterations almost in all studied parameters, substantially decreasing cell viability and ATP level and altering the size and granularity of tested cells; in contrast, PFHxA and PFBA induced significant changes only at some studied parameters. PFOA also induced a notable increase in intracellular ROS and RNS levels, which suggest that both oxidative stress and nitrosative stress influence its cytotoxic potential. Interestingly, the shortest-chain compound, PFBA, induced changes that were not observed for PFHxA. This suggests that the length of the chain determines the triggering of certain alterations in PBMCs. Importantly, the changes were noted at concentrations corresponding to those associated with occupational exposure. These findings contribute to our understanding of the immunotoxicity of PFOA and its substitutes, indicating the potential health risks associated with chronic exposure, particularly in populations with occupational exposure or high environmental PFOA burdens. Full article

Hans Selye’s stress concept, first introduced in the 1930s, has undergone substantial evolution, extending beyond biology and medicine to influence diverse academic disciplines. Initially, Selye’s General Adaptation Syndrome (GAS) described nonspecific physiological responses to stressors exclusively in mammals, without addressing other biological systems. Consequently, the concept of stress developed independently in biology and medicine, shaped by distinct physiological contexts. This review provides a historical overview of stress research, highlights both parallels and divergences between the stress responses of plants and animals, and integrates insights from traditional Eastern philosophies. We propose an updated GAS framework that incorporates the dynamic balance among reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive sulfur species (RSS) within the broader context of oxidative stress. We highlight the ionotropic glutamate receptor (iGluR) family and the transient receptor potential (TRP) channel superfamily as minimal molecular architectures for achieving GAS. This perspective expands the classical stress paradigm, providing new insights into redox biology, interspecies stress adaptation, and evolutionary physiology. Full article

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. Increasing evidence highlights oxidative stress as a pivotal contributor to AD pathogenesis, closely associated with hallmark features such as amyloid-β (Aβ) plaque accumulation, tau hyperphosphorylation, and synaptic dysfunction. This review aims to elucidate the mechanisms by which oxidative stress contributes to AD and to evaluate emerging therapeutic strategies targeting oxidative damage. Methods: We conducted an extensive literature search using PubMed and Google Scholar for studies published between 1994 and 2024. This narrative review integrates findings from in vitro, in vivo, and clinical studies focusing on oxidative stress, mitochondrial dysfunction, and their roles in AD to provide a comprehensive overview of the current research landscape. Results: ROS and RNS levels are significantly elevated in aging and AD-affected brains, leading to oxidative damage to lipids, proteins, and DNA, which compromises neuronal function and structure. Mitochondrial dysfunction plays a key role by amplifying ROS production, impairing ATP synthesis, and accelerating neurodegeneration. Oxidative stress also interacts with central AD pathologies, including Aβ aggregation, tau hyperphosphorylation, and synaptic dysfunction, creating a vicious cycle of neuronal injury. Although traditional antioxidant therapies have shown limited efficacy in clinical settings, often due to poor bioavailability, limited BBB penetration, and systemic distribution, novel strategies such as mitochondrial-targeted antioxidants and combination therapies have demonstrated improved outcomes in preclinical models. Conclusions: Oxidative stress plays a multifaceted role in the progression of AD, necessitating comprehensive therapeutic approaches. Future treatments should focus on targeting multiple aspects of oxidative stress, particularly mitochondrial dysfunction, to enhance clinical outcomes and slow neurodegeneration in AD patients. Full article

Shock is a life-threatening condition characterized by inadequate tissue perfusion leading to systemic hypoxia and metabolic failure. Ischemia/reperfusion (I/R) injury exacerbates shock progression through oxidative stress and immune dysregulation, contributing to multi-organ dysfunction. This narrative review synthesizes current evidence on the interplay between I/R injury, oxidative stress, and immune modulation in shock states. We analyze the classification of shock, its progression, and the molecular pathways involved in ischemic adaptation, inflammatory responses, and oxidative injury. Shock pathophysiology is driven by systemic ischemia, triggering adaptive responses such as hypoxia-inducible factor (HIF) signaling and metabolic reprogramming. However, prolonged hypoxia leads to mitochondrial dysfunction, increased reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, and immune activation. The transition from systemic inflammatory response syndrome (SIRS) to compensatory anti-inflammatory response syndrome (CARS) contributes to immune imbalance, further aggravating tissue damage. Dysregulated immune checkpoint pathways, including CTLA-4 and PD-1, fail to suppress excessive inflammation, exacerbating oxidative injury and immune exhaustion. The intricate relationship between oxidative stress, ischemia/reperfusion injury, and immune dysregulation in shock states highlights potential therapeutic targets. Strategies aimed at modulating redox homeostasis, controlling immune responses, and mitigating I/R damage may improve patient outcomes. Future research should focus on novel interventions that restore immune balance while preventing excessive oxidative injury. Full article

Mitochondria play a central role in energy metabolism and continuously adapt through dynamic processes such as fusion and fission. When the balance between these processes is disrupted, it can lead to mitochondrial dysfunction and increased oxidative stress, contributing to the development and progression of various cardiometabolic diseases (CMDs). Their role is crucial in diabetes mellitus (DM), since their dysfunction drives β-cell apoptosis, immune activation, and chronic inflammation through excessive ROS production, worsening endogenous insulin secretion. Moreover, sympathetic nervous system activation and altered dynamics, contribute to hypertension through oxidative stress, impaired mitophagy, endothelial dysfunction, and cardiomyocyte hypertrophy. Furthermore, the role of mitochondria is catalytic in endothelial dysfunction through excessive reactive oxygen species (ROS) production, disrupting the vascular tone, permeability, and apoptosis, while impairing antioxidant defense and promoting inflammatory processes. Mitochondrial oxidative stress, resulting from an imbalance between ROS/Reactive nitrogen species (RNS) imbalance, promotes atherosclerotic alterations and oxidative modification of oxidizing low-density lipoprotein (LDL). Mitochondrial DNA (mtDNA), situated in close proximity to the inner mitochondrial membrane where ROS are generated, is particularly susceptible to oxidative damage. ROS activate redox-sensitive inflammatory signaling pathways, notably the nuclear factor kappa B (NF-κB) pathway, leading to the transcriptional upregulation of proinflammatory cytokines, chemokines, and adhesion molecules. This proinflammatory milieu promotes endothelial activation and monocyte recruitment, thereby perpetuating local inflammation and enhancing atherogenesis. Additionally, mitochondrial disruptions in heart failure promote further ischemic injury and excessive oxidative stress release and impair ATP production and Ca²⁺ dysregulation, contributing to cell death, fibrosis, and decreased cardiac performance. This narrative review aims to investigate the intricate relationship between mitochondrial dysfunction and CMDs. Full article

Influenza A virus (IAV) is an important respiratory pathogen. We evaluated the IAV-inactivation activity of hydroxytyrosol (HT)-rich aqueous olive pulp extract (HIDROX^®) and its mechanisms. The HIDROX-containing solution and cream showed concentration- and time-dependent virucidal activity. The virucidal activity of HIDROX was higher than pure HT. With Western blotting (WB), the band intensities of multiple viral structural proteins in HIDROX- and HT-treated viruses were weaker than in the control, and high-molecular-mass bands were observed. These results suggest that HIDROX and HT may have induced the structural changes or abnormalities of viral proteins. HIDROX and HT had no or limited impact on hemagglutination and neuraminidase activities, as well as the virus genome. No apparent abnormalities in the viral particles were observed through electron microscopy following treatment with HIDROX and HT. Treatment with HT, but not HIDROX, resulted in the production of high levels of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS). In HT treatment but not HIDROX treatment, the virucidal activity disappeared, and the induction of abnormal band patterns of a viral protein in WB was cancelled by ROS/RNS scavenger activity. These findings showed the possible utility of HIDROX as a naturally derived IAV virucidal component that may contribute to IAV control. Full article