Search Results (329)

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

Seed germination and early seedling growth are pivotal stages that define crop establishment and yield potential. Conventional agrochemicals used to improve these processes often raise environmental concerns, highlighting the need for sustainable alternatives. In this study, we demonstrated that water treated with cylindrical dielectric barrier discharge (c-DBD) plasma, enriched with nitric oxide (NO) and reactive nitrogen species (RNS), markedly enhanced onion (Allium cepa) seed germination and seedling vigor. The plasma-treated water (PTW) promoted rapid imbibition, broke dormancy, and accelerated germination rates beyond 98%. Seedlings irrigated with PTW exhibited significantly increased biomass, root and shoot length, chlorophyll content, and antioxidant enzyme activities, accompanied by reduced lipid peroxidation. Transcriptomic profiling revealed that PTW orchestrated a multifaceted regulatory network by upregulating gibberellin biosynthesis genes (GA3OX1/2), suppressing abscisic acid signaling components (ABI5), and activating phenylpropanoid metabolic pathways (PAL, 4CL) and antioxidant defense genes (RBOH1, SOD). These molecular changes coincided with elevated NO₂⁻ and NO₃⁻ levels and finely tuned hydrogen peroxide dynamics, underpinning redox signaling crucial for seed activation and stress resilience. Our findings establish plasma-generated NO-enriched water as an innovative, eco-friendly technology that leverages redox and hormone crosstalk to stimulate germination and early growth, offering promising applications in sustainable agriculture. 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

Reactive nitrogen species (RNS), particularly peroxynitrite (ONOO⁻), play a central role in post-translational modifications (PTMs) of proteins, including fibrinogen, a key component of the coagulation cascade. This review explores the structural and functional consequences of fibrinogen nitration, with a focus on its impact on clot formation, morphology, mechanical stability, and fibrinolysis. Nitration, primarily targeting tyrosine residues within functional domains of the Aα, Bβ, and γ chains, induces conformational changes, dityrosine crosslinking, and aggregation into high molecular weight species. These modifications result in altered fibrin polymerization, the formation of porous and disorganized clot networks, reduced mechanical resilience, and variable susceptibility to fibrinolysis. Moreover, nitrated fibrinogen may affect interactions with platelets and endothelial cells, although current evidence remains limited. Emerging clinical studies support its role as both a prothrombotic mediator and a potential biomarker of oxidative stress in cardiovascular and inflammatory diseases. Finally, we explore both pharmacological interventions, such as NOX inhibitors, and natural antioxidant strategies at counteracting fibrinogen nitration. Overall, fibrinogen nitration emerges as a critical molecular event linking oxidative stress to thrombotic risk. 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

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

Background/Objectives: Oral health is a complex concept involving physical, psychological, emotional, and social components. A key factor in maintaining oral tissue integrity is redox balance, which is disrupted by oxidative stress (OS) through an imbalance between reactive oxygen species (ROS) and antioxidant defenses. This study examines the contribution of endogenous and exogenous sources to OS and explores the therapeutic potential of medicinal plants from the Asteraceae and Lamiaceae families in restoring redox homeostasis and improving oral health. Methods: A literature review was conducted, analyzing the role of OS in oral diseases and the antioxidant mechanisms of selected Asteraceae species. Special attention was given to their phytochemical contents—polyphenols, flavonoids, and essential oils—and their biological relevance to oral health. Results: OS plays a critical role in the onset and progression of oral conditions such as caries, periodontitis, gingivitis, aphthous ulcers, abscesses, precancerous lesions, and oral cancers. ROS and reactive nitrogen species (RNS) cause inflammation, tissue breakdown, and salivary gland dysfunction. Asteraceae plants like Matricaria chamomilla, Calendula officinalis, Cichorium intybus, Taraxacum officinale, Arctium lappa, Achillea millefolium, and Solidago virgaurea demonstrate notable antioxidant, anti-inflammatory, and antimicrobial properties that help counteract OS and support oral homeostasis. Conclusions: Asteraceae and Lamiaceae species show high therapeutic potential in addressing OS-related oral disorders. Their bioactive compounds aid in restoring redox balance and protecting oral tissues. These findings support the integration of phytotherapeutic agents into oral healthcare and call for further clinical validation of plant-based strategies for disease prevention and management. Full article

Peroxynitrite (ONOO⁻) is a reactive nitrogen species (RNS) that plays pivotal roles in various physiological and pathological processes. The recent literature has seen significant progress in the development of highly sensitive and selective fluorescent probes applicable for monitoring ONOO⁻ dynamics in live cells and a variety of animal models of human diseases. However, the clinical applications of those probes remain much less explored. This review delves into the biological roles of ONOO⁻ and summarizes the design strategies, sensing mechanisms, and bioimaging applications of near-infrared (NIR), long-wavelength, two-photon, and ratiometric fluorescent probes modified with a diverse range of functional groups responsive to ONOO⁻. Furthermore, we will discuss the remaining problems that prevent the currently developed ONOO⁻ probes from translating into clinical practice. Full article

Cold atmospheric plasma (CAP) acts as a powerful antibacterial tool in the food industry, effectively eliminating E. coli and a wide range of pathogens, including bacteria, viruses, fungi, spores, and biofilms in meat and vegetables. Unlike traditional bactericidal methods, CAP leverages an arsenal of reactive species, including reactive oxygen species (ROS) such as ozone (O3) and hydroxyl radicals (OH•), and reactive nitrogen species (RNS) like nitric oxide (NO•), alongside UV radiation and charged particles. These agents synergistically dismantle E. coli’s cell membranes, proteins, and DNA, achieving high degradation rates without thermal or chemical damage to processed food. This non-thermal, eco-friendly technology preserves food’s nutritional and sensory integrity, offering a transformative edge over conventional approaches. It emphasizes the critical need to optimize treatment parameters (exposure time, gas composition, power) to unlock CAP’s full potential. This review explores CAP’s effectiveness in degrading E. coli, emphasizing the optimization of treatment parameters for practical food industry applications and its potential as a scalable food safety solution. It is crucial to conduct further studies to enhance its implementation, establishing CAP as a fundamental element of advanced food processing technologies and a key measure for protecting public health. Full article

Cellular senescence plays a pivotal role in aging and stress response mechanisms. Controlling cellular senescence is essential for developing novel techniques to prevent aging or aging-related diseases and promote a healthy lifespan. This study explores the efficiency of cold atmospheric microplasma (CAM) for controlling cellular senescence in yeast Saccharomyces cerevisiae. Reactive oxygen and nitrogen species (RONS) generated by CAM influence key processes, such as the regulation of oxidative stress, alterations in membrane potential, and senescence-related epigenetic modifications. As a marker of cellular senescence, the expression of β-galactosidase was assessed in response to different plasma treatments. At a frequency of 1 kHz and a discharge voltage of 5 kV_p-p, a significant reduction in β-galactosidase activity was observed in cells treated for 10 s and 30 s compared to the control, indicating a reduction in cellular senescence. Additionally, cell viability, metabolic activity, and plasma membrane potential were also found to be higher for the treated cells compared to the control under the same conditions. This study confirms that a physiologically tolerable level of ROS and RNS is sufficient for cellular signaling, but not for damage induction. The findings from this study provide insights on the potential of microplasma as a tool for controlling cellular senescence and the development of therapeutic innovations involving eukaryotic cells. Full article