Role Of Reactive Oxygen Species Research Articles

Self-driven microplasma decontaminates chemical warfare agent simulant in different gas environments

To develop and refine a self-driven plasma decontamination system, this study investigated the effect of different gas environments (air, Ar, Ar/O2, and Ar/O2/H2O) on the degradation efficiency of 2-chloroethyl ethyl sulfide (2-CEES). A dielectric-dielectric rotating triboelectric nanogenerator (dd-rTENG) was constructed to mechanically induce atmospheric plasma. The dominant active species of different plasmas were identified through spectroscopic and chemical probe diagnostic methods. The results revealed that Ar/O2 and Ar/O2/H2O plasmas generated higher levels of reactive Ox species (O3, O2-, and 1O2) and OH radicals, respectively. Notably, the Ar/O2 and Ar/O2/H2O plasmas exhibited significantly higher decontamination efficiencies than the other plasmas. Moreover, the Ar/O2/H2O plasma featured an energy utilization efficiency of 0.962 μg/J, which is nearly twice that of the previously reported study. However, the Ar plasma exhibited minimal decontamination effect owing to its low electron energy and absence of active species. Further studies have indicated the vital role of reactive oxygen species in the 2-CEES decontamination process. Active Ox can promote the oxidation of 2-CEES, while OH can effectively mitigate the peroxidation process. Furthermore, the system exhibited low electron energy, which might play small role for 2-CEES decontamination. This study is vital for developing self-driven plasma decontamination devices and provides significant clues for understanding the 2-CEES decontamination mechanism.

Biology of cognitive aging across species.

Aging is associated with cognitive decline, which can critically affect quality of life. Examining the biology of cognitive aging across species will lead to a better understanding of the fundamental mechanisms involved in this process, and identify potential interventions that could help to improve cognitive function in aging individuals. This minireview aimed to explore the mechanisms and processes involved in cognitive aging across a range of species, from flies to rodents, and covers topics, such as the role of reactive oxygen species and autophagy/mitophagy in cognitive aging. Overall, this literature provides a comprehensive overview of the biology of cognitive aging across species, highlighting the latest research findings and identifying potential avenues for future research. Geriatr Gerontol Int 2024; 24: 15-24.

LIVING LONGER WITH MODERATE AMOUNTS OF OXYGEN RADICALS IN FRUIT FLIES

Abstract The role of reactive oxygen species (ROS) in aging is complex and paradoxical. While the free radical theory of aging suggests that ROS cause cellular damage and senescence, some studies have shown that moderate ROS levels can enhance cellular adaptation and longevity. In this research, we used Drosophila as an in vivo model to investigate the optimal level of ROS that can promote healthy aging. We exposed flies to different concentrations of paraquat (PQ), a herbicide that generates superoxide anions, and measured their lifespan, stress resistance, and gene expression. We found that intermediate PQ levels (0.1 mM) extended lifespan and improved stress tolerance, while high PQ levels (0.5 mM) shortened lifespan and impaired stress response. We also observed an up-regulation of ROS scavenger genes, such as superoxide dismutase 1 and glutathione peroxidase, in the intermediate PQ group, suggesting a homeostatic mechanism to balance ROS levels. Our findings challenge the conventional view of ROS as harmful agents and provide novel insights into the molecular mechanisms of aging.

The role of Reactive Oxygen Species (ROS) in the Nandrolone-Decanoate-induced liver fibrosis

To determine the role of reactive oxygen species (ROS) and its relationship with tumor necrosis factor-alpha (TNF-alpha) during the process of developing liver fibrosis induced by Nandrolone Decanoate, 36 adult male Wistar rats are divided into 3 groups. Except for the control group, the other 2 experimental groups are injected with nandrolone decanoate (3.5 mg/kg/5 times/IM/week) for 4 weeks. After 4 weeks of injection, one experimental group (A) is decapitated. Samples from livers and plasma are obtained to conduct histopathological section, TNF-alpha ELISA, and EPR for ROS level. Then along with the same dosage of nandrolone decanoate, raxofelast (15mg/kg/day) is administrated orally to the experimental group (B) for another 4 weeks. The result of the histopathology section, ELISA, and EPR tests of group A and group B were compared. The degree of liver fibrosis, reactive oxygen species amount, and TNF-alpha level before and after the administration of antioxidants indicate the role of ROS in the development of TNF-alpha-mediated liver fibrosis. Another purpose of this experiment is to discuss the potential of antioxidants in the treatment of steroid-induced liver fibrosis.

Reduced Zn2+ promotes retinal ganglion cells survival and optic nerve regeneration after injury through inhibiting autophagy mediated by ROS/Nrf2

The molecular mechanism of how reduced mobile zinc (Zn2+) affected retinal ganglion cell (RGC) survival and optic nerve regeneration after optic nerve crush (ONC) injury remains unclear. Here, we used conditionally knocked out ZnT-3 in the amacrine cells (ACs) of mice (CKO) in order to explore the role of reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (NFE2L2, Nrf2) and autophagy in the protection of RGCs and axon regeneration after ONC injury. We found that reduced Zn2+ can promote RGC survival and axonal regeneration by decreasing ROS, activating Nrf2, and inhibiting autophagy. Additionally, autophagy after ONC is regulated by ROS and Nrf2. Visual function in mice after ONC injury was partially recovered through the reduction of Zn2+, achieved by using a Zn2+ specific chelator N,N,Nʹ,Nʹ-tetrakis-(2-Pyridylmethyl) ethylenediamine (TPEN) or through CKO mice. Overall, our data reveal the crosstalk between Zn2+, ROS, Nrf2 and autophagy following ONC injury. This study verified that TPEN or knocking out ZnT-3 in ACs is a promising therapeutic option for the treatment of optic nerve damage and elucidated the postsynaptic molecular mechanism of Zn2+-triggered damage to RGCs after ONC injury.

Oxidative Stress and the Pathogenesis of Aortic Aneurysms.

Aortic aneurysms are responsible for significant morbidity and mortality. Despite their clinical significance, there remain critical knowledge gaps in the pathogenesis of aneurysm disease and the mechanisms involved in aortic rupture. Recent studies have drawn attention to the role of reactive oxygen species (ROS) and their down-stream effectors in chronic cardiovascular diseases and specifically in the pathogenesis of aortic aneurysm formation. This review will discuss current mechanisms of ROS in mediating aortic aneurysms, the failure of endogenous antioxidant systems in chronic vascular diseases, and their relation to the development of aortic aneurysms.

ROS-scavenging materials for skin wound healing: advancements and applications.

The intricate healing process of skin wounds includes a variety of cellular and molecular events. Wound healing heavily relies on reactive oxygen species (ROS), which are essential for controlling various processes, including inflammation, cell growth, angiogenesis, granulation, and the formation of extracellular matrix. Nevertheless, an overabundance of reactive oxygen species (ROS) caused by extended oxidative pressure may result in the postponement or failure of wound healing. It is crucial to comprehend the function of reactive oxygen species (ROS) and create biomaterials that efficiently eliminate ROS to enhance the healing process of skin wounds. In this study, a thorough examination is presented on the role of reactive oxygen species (ROS) in the process of wound healing, along with an exploration of the existing knowledge regarding biomaterials employed for ROS elimination. In addition, the article covers different techniques and substances used in the management of skin wound. The future prospects and clinical applications of enhanced biomaterials are also emphasized, highlighting the potential of biomaterials that scavenge active oxygen to promote skin repair. This article seeks to enhance the understanding of the complex processes of ROS in the healing of wounds and the application of ROS-scavenging materials. Its objective is to create novel strategies for effective treatment skin wounds.

The Role of Reactive Oxygen Species in the In Vitro Germination and Growth of the Petunia (Petunia hybrida E. Vilm.) Male Gametophyte

The in vitro growth of the pollen tube (PT), an object of comprehensive and intensive research, is a model for studying the mechanisms of sexual reproduction in higher plants. We have studied the potential role of reactive oxygen species (ROS) in the in vitro germination and growth maintenance of the petunia (Petunia hybrida E. Vilm.) male gametophyte. The exogenous treatment with H2O2 influences the PT germination and polar growth in vitro. The addition of H2O2 to culture medium increases both the percentage of pollen grain germination and the PT length in the case of long cultivation, but inhibits both processes during the first hour of cultivation. This suggests that endogenous ROS play a decisive role in the early stages of pollen germination, with the sensitivity to endogenous ROS emerging later over the course of their growth. The addition of diphenylene iodonium chloride (DPI), a NADPH oxidase inhibitor, considerably decreases both the germination and the growth of the petunia male gametophyte at low concentrations (0.1 μM), and completely arrests the growth at high concentrations (1 μM). ROS are necessary for polar growth of the petunia male gametophyte; they are secreted in the early stages of pollen grain activation and are further localized to the initiation of the PT, mainly in the PT apical part, during polar growth, as confirmed with the help of intravital fluorescence microscopy.

Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells.

Microplastics (MPs) have attracted widespread worldwide attention as a new pollutant. However, the role of reactive oxygen species (ROS) and cell cycle in nephrotoxicity induced by different concentrations of polystyrene microplastics (PS-MPs) is unknown. This study used grass carp kidney cells (CIK) treated with different concentrations of PS-MPs (0, 0.012, 0.0625, and 0.5 mg L-1 ) as subjects. With the increase of PS-MPs concentration, the levels of ROS and malonaldehyde increased, while the level of total antioxidant capacity, superoxide Dismutase (SOD), and glutathione (GSH) activity decreased. The expression of BUB1 mitotic checkpoint serine/threonine kinase (BUB1), cyclin-dependent kinase (CDK1), CDK2, CyclinB1, cell division cycle 20 homolog (CDC20), and B-cell lymphoma-2, sequestosome 1 decreased significantly. Nevertheless, the expression of Caspase 3, Cleave-Caspase 3, cytochrome c (Cytc), BCL2-associated X, apoptosis regulator, poly ADP-ribose polymerase (PARP), Cleave-PARP, Caspase 9, autophagy immunoblot kit (LC3), and Beclin1 increased. Our research shows that PS-MPs can trigger oxidative stress and induce cell cycle arrest, apoptosis, and autophagy in CIK cells by regulating ROS. This work provides a theoretical basis for cellular biology and toxicology mechanisms and new insights into the potential risks to animals from MPs exposure in the environment.

Aspergillus Enhances Eosinophil and Neutrophil Extracellular DNA Trap Formation in Chronic Rhinosinusitis.

Chronic rhinosinusitis (CRS) is characterized by inflammatory cell infiltration in the sinonasal mucosa. Eosinophil and neutrophil extracellular traps (EETs and NETs, respectively) are prominently found in CRS. This study aimed to investigate the effect of airborne fungi, Alternaria alternata and Aspergillus fumigatus, on EET and NET formation. Nasal epithelial cells, eosinophils, and neutrophils were isolated from eosinophilic CRS (ECRS), non-ECRS (NECRS), and healthy control. We determined eosinophil and neutrophil transepithelial migration after fungal treatment. We then determined the release of EETs and NETs by fungi using Sytox Green staining and determined the role of reactive oxygen species (ROS) using ROS inhibitors. We identified more abundant EETs and NETs in ECRS than in NECRS. A. alternata and A. fumigatus enhanced eosinophil and neutrophil transepithelial migration. A. fumigatus strongly induced EET and NET formation in CRS and, simultaneously, suppressed fungal metabolic activity. EET formation in CRS is associated with nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase and NET formation with NADPH-oxidase and mitochondrial ROS. A. fumigatus, but not A. alternata, induced EET and NET formation, and peripheral blood eosinophils and neutrophils exhibited different immune responses against A. fumigatus following the inflammatory status of the host. Aspergillus-fumigatus-induced EET and NET formation plays a crucial role in CRS pathogenesis.

Photoelectrocatalytic Processes of TiO2 Film: The Dominating Factors for the Degradation of Methyl Orange and the Understanding of Mechanism.

Various thicknesses of TiO2 films were prepared by the sol-gel method and spin-coating process. These prepared TiO2 films exhibit thickness-dependent photoelectrochemical performance. The 1.09-μm-thickTiO2 film with 20 spin-coating layers (TiO2-20) exhibits the highest short circuit current of 0.21 mAcm-2 and open circuit voltage of 0.58 V among all samples and exhibits a low PEC reaction energy barrier and fast kinetic process. Photoelectrocatalytic (PEC) degradation of methyl orange (MO) by TiO2 films was carried out under UV light. The roles of bias, film thickness, pH value, and ion properties were systematically studied because they are the four most important factors dominating the PEC performance of TiO2 films. The optimized values of bias, film thickness, and pH are 1.0 V, 1.09 μm, and 12, respectively, which were obtained according to the data of the PEC degradation of MO. The effect of ion properties on the PEC efficiency of TiO2-20 was also analyzed by using halide as targeted ions. The "activated" halide ions significantly promoted the PEC efficiency and the order was determined as Br > Cl > F. The PEC efficiency increased with increasing Cl content, up until the optimized value of 30 × 10-3 M. Finally, a complete degradation of MO by TiO2-20 was achieved in 1.5 h, with total optimization of the four factors: 1.0 V bias, 1.09-μm-thick, pH 12, and 30 × 10-3 M Cl ion content. The roles of reactive oxygen species and electric charge of photoelectrodes were also explored based on photoelectrochemical characterizations and membrane-separated reactors. Hydrogen peroxide, superoxide radical, and hydroxyl radical were found responsible for the decolorization of MO.

Role of reactive oxygen species: In the cytotoxicity and apoptosis of colon cancer cell line due to green lead nanoparticles

Nanoparticles are involved in regulating the biology of cancer cell treatment, but their mechanism is not fully understood. We synthesized and characterized new green lead nanoparticles (gPbNPs) by using an extract of Ziziphus spina christi leaves. Its cytotoxic and apoptotic effect on the human colon cancer Cacoa2 cell line was evaluated. The gPbNPs were characterized by using energy dispersive X-rays, scanning electron microscopes, and transmission electron microscopes. The cytotoxic effects of gPbNPs against the human colon cancer Cacoa2 cell line were investigated, as were the possible mechanisms underlying the induction of apoptosis. In this experiment, we observed the production of intracellular reactive oxygen species (ROS) in cells, and the installation of caspase 3/7 was higher in cells at 16 µg/mL of gPbNPs. Moreover, the Bax gene was upregulated and the Bcl2 gene was downregulated, and increased caspase-3/7 activity confirmed the apoptotic effect of gPbNPs in cells. The cytotoxicity test confirmed that gPbNPs were selectively toxic in cancer cells and induced apoptosis by activating bad, bax, caspase-3/7, p27, p53 protein, and proteins involved in apoptosis. Our observation showed that gPbNPs induced cell toxicity, increased generation of intracellular ROS, and gene expression of Bcl2, and Bax, in the Cacoa2 cell line. In conclusion, these findings demonstrated that gPbNPs executed toxic effects on the Cacoa2 cell line by activating caspase-3/7 activity.

The Role of Reactive Oxygen Species in the Regulation of Blood Vessel Tone in Perinatal and Early Postnatal Ontogenesis

Reactive oxygen species (ROS) have been considered for many years as negative regulators in the cardiovascular system. Indeed, excessive production of ROS characterizes many cardiovascular diseases. The damaging effect of ROS can be especially pronounced in a newborn organism, since during this period their contractile effect in pulmonary arteries remains as high as in the pre-term fetus arteries and the antioxidant systems have not yet formed. Therefore, in the first hours and days of independent life, pulmonary arteries tend to contract, primarily due to the low bioavailability of endothelial NO, which increases the risk of developing pulmonary hypertension in newborns. At the same time, during the perinatal period, ROS play an important role in the adaptive reactions of the circulatory system. ROS provide occlusion of the ductus arteriosus and separation of the pulmonary and systemic circulations soon after birth, and also contribute to the contraction of peripheral vessels during hypoxia, which often accompanies the delivery, and therefore provide priority blood supply to the brain in these conditions. The vasomotor effect of ROS is also pronounced in early postnatal ontogenesis, but it has a different character. In the first weeks of life, the action of ROS serves as one of the mechanisms for increasing endothelium-dependent relaxation of pulmonary vessels. In addition, during early postnatal ontogeny, ROS may play an important role in the regulation of systemic vascular tone. This review outlines the current understanding of the vasomotor role of ROS in the vessels of the pulmonary and systemic circulation and considers the mechanisms of ROS effects on the functioning of vascular endothelial and smooth muscle cells in the perinatal and early postnatal periods.

Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension.

Pulmonary hypertension (PH) resulting from chronic hypoxia (CH) occurs in patients with chronic obstructive pulmonary diseases, sleep apnea, and restrictive lung diseases, as well as in residents at high altitude. Previous studies from our group and others demonstrate a detrimental role of reactive oxygen species (ROS) in the pathogenesis of CH-induced PH, although the subcellular sources of ROS are not fully understood. We hypothesized that mitochondria-derived ROS (mtROS) contribute to enhanced vasoconstrictor reactivity and PH following CH. To test the hypothesis, we exposed rats to 4 weeks of hypobaric hypoxia (PB ≈ 380 mmHg), with control rats housed in ambient air (PB ≈ 630 mmHg). Chronic oral administration of the mitochondria-targeted antioxidant MitoQ attenuated CH-induced decreases in pulmonary artery (PA) acceleration time, increases in right ventricular systolic pressure, right ventricular hypertrophy, and pulmonary arterial remodeling. In addition, endothelium-intact PAs from CH rats exhibited a significantly greater basal tone compared to those from control animals, as was eliminated via MitoQ. CH also augmented the basal tone in endothelium-disrupted PAs, a response associated with increased mtROS production in primary PA smooth muscle cells (PASMCs) from CH rats. However, we further uncovered an effect of NO synthase inhibition with Nω-nitro-L-arginine (L-NNA) to unmask a potent endothelial vasoconstrictor influence that accentuates mtROS-dependent vasoconstriction following CH. This basal tone augmentation in the presence of L-NNA disappeared following combined endothelin A and B receptor blockade with BQ123 and BQ788. The effects of using CH to augment vasoconstriction and PASMC mtROS production in exogenous endothelin 1 (ET-1) were similarly prevented by MitoQ. We conclude that mtROS participate in the development of CH-induced PH. Furthermore, mtROS signaling in PASMCs is centrally involved in enhanced pulmonary arterial constriction following CH, a response potentiated by endogenous ET-1.

Constructive Z-scheme interfacial charge transfer of a spinel ferrite-supported g-C3N4 heterojunction architect for photocatalytic degradation

The design and fabrication of metal ferrite-supported porous g-C3N4 (p-GCN) tandem heterojunctions constructed via the hydrothermal method. Phase identification, morphology, magnetic, thermal, and electrochemical properties were studied. The physicochemical characteristic studies confirmed the effective interaction and formation of the heterojunction architect. The fabricated materials were employed as a photocatalyst for the degradation of rhodamine B (RhB), tetracycline (TC), cartap hydrochloride (C-HCl), and complex effluent (RhB+TC+C-HCl) under sunlight irradiation. The p-GCN/AgFe2O4 (p-GCN/AFO) heterojunction demonstrates outstanding performance within 60 min of irradiation (RhB- 98.3%, TC- 98.5%, C-HCl- 99.56%, and complex effluent- 95.72%), whereas p-GCN/MgFe2O4 (p-GCN/MFO) shows slightly reduced activity (RhB- 97.14%, TC- 97.62%, C-HCl- 99.23%, and complex effluent- 91.05%). The performance improvement of nanocomposites is due to complementary sunlight absorption, sequential energy, and electron transfer properties, efficient charge separation, and excellent redox potential of its heterojunction structure. Furthermore, a thorough mechanism analysis suggests the essential role of reactive oxygen species (•OH and •O2-) and it is proposed that the nanocomposite photocatalyst follows a Z-scheme heterojunction mechanism. The high catalytic activity, the magnetic recoverability, and the excellent stability of p-GCN/AFO make it a potential candidate for the degradation of multiple organic contaminants in various industry sectors.

The Underexplored Mechanisms of Wheat Resistance to Leaf Rust

Wheat leaf rust, caused by the obligate biotrophic fungus Puccinia triticina Eriks. (Pt), is one of the most common wheat foliar diseases that continuously threatens global wheat production. Currently, the approaches used to mitigate pathogen infestation include the application of fungicides and the deployment of resistance genes or cultivars. However, the continuous deployment of selected resistant varieties causes host selection pressures that drive Pt evolution and promote the incessant emergence of new virulent races, resulting in the demise of wheat-resistant cultivars after several years of planting. Intriguingly, diploid wheat accessions were found to confer haustorium formation-based resistance to leaf rust, which involves prehaustorial and posthaustorial resistance mechanisms. The prehaustorial resistance in the interaction between einkorn and wheat leaf rust is not influenced by specific races of the pathogen. The induced defense mechanism, known as systemic acquired resistance, also confers durable resistance against a wide array of pathogens. This review summarizes the host range, pathogenic profile, and evolutionary basis of Pt; the molecular basis underlying wheat–Pt interactions; the cloning and characterization of wheat leaf rust resistance genes; prehaustorial and posthaustorial resistance; systemic acquired resistance; and the role of reactive oxygen species. The interplay between climatic factors, genetic features, planting dates, and disease dynamics in imparting resistance is also discussed.

Nitrogen-deficient leaves and roots can keep high abilities to scavenge reactive oxygen species and methylglyoxal, and protect them against oxidative damage in Citrus sinensis seedlings

Nitrogen-deficiency (ND) usually occurs in some citrus orchard soils in China. The roles of reactive oxygen species (ROS) and methylglyoxal (MG) generation and their detoxification systems in ND tolerance of horticultural woody plants still need to be revealed. For the first time, we examined the effects of ND on ROS and MG generation and their detoxification systems in leaves and roots of Citrus sinensis seedlings. The objectives are to test the hypotheses that N-deficient leaves and roots can keep high abilities to scavenge ROS and MG, thereby protecting them from oxidative damage, and that ND-induced alterations of ROS and MG formation and their detoxification systems in leaves and roots are different. ND augmented superoxide anion production rate and MG concentrations, but it decreased malondialdehyde (MDA) concentrations and electrolyte leakage in leaves and roots. ND increased the activities of most enzymes involved in ROS (ascorbate-glutathione cycle-related enzymes, antioxidant enzymes, and sulfur metabolism-related enzymes) and MG (glyoxalases) detoxification expressed on a protein basis with a few exceptions, and the concentrations of ascorbate, phytochelatins, and total non-protein thiols in leaves and roots. These results suggested that nitrogen-deficient leaves and roots could keep high abilities to detoxify ROS and MG, and protect them from oxidative damage. Generally viewed, ND affected the production and removal of ROS and MG more in roots than in leaves.

NINJ1 is activated by cell swelling to regulate plasma membrane permeabilization during regulated necrosis

Plasma membrane permeabilization (PMP) is a defining feature of regulated necrosis. It allows the extracellular release of damage-associated molecular patterns (DAMPs) that trigger sterile inflammation. The pore forming molecules MLKL and GSDMs drive PMP in necroptosis and pyroptosis, respectively, but the process of PMP remains unclear in many other forms of regulated necrosis. Here, we identified NINJ1 as a crucial regulator of PMP and consequent DAMP release during ferroptosis, parthanatos, H2O2-induced necrosis and secondary necrosis. Importantly, the membrane-permeabilizing function of NINJ1 takes place after the metabolic death of the cells and is independent of the pore-forming molecules MLKL, GSDMD and GSDME. During ferroptosis, NINJ1 acts downstream of lipid peroxidation, which suggested a role for reactive oxygen species (ROS) in NINJ1 activation. Reactive oxygen species were however neither sufficient nor required to trigger NINJ1-dependent PMP. Instead, we found that NINJ1 oligomerization is induced by the swelling of the cell and that its permeabilizing potential still requires an addition, and yet to be discovered, activation mechanism.

Reactive Oxygen Species and Strategies for Antioxidant Intervention in Acute Respiratory Distress Syndrome.

Acute respiratory distress syndrome (ARDS) is a life-threatening pulmonary condition characterized by the sudden onset of respiratory failure, pulmonary edema, dysfunction of endothelial and epithelial barriers, and the activation of inflammatory cascades. Despite the increasing number of deaths attributed to ARDS, a comprehensive therapeutic approach for managing patients with ARDS remains elusive. To elucidate the pathological mechanisms underlying ARDS, numerous studies have employed various preclinical models, often utilizing lipopolysaccharide as the ARDS inducer. Accumulating evidence emphasizes the pivotal role of reactive oxygen species (ROS) in the pathophysiology of ARDS. Both preclinical and clinical investigations have asserted the potential of antioxidants in ameliorating ARDS. This review focuses on various sources of ROS, including NADPH oxidase, uncoupled endothelial nitric oxide synthase, cytochrome P450, and xanthine oxidase, and provides a comprehensive overview of their roles in ARDS. Additionally, we discuss the potential of using antioxidants as a strategy for treating ARDS.

Current trends in targeting the oxidative stress in glaucoma (Review).

Glaucoma is a progressive optic neuropathy characterised by retinal ganglion cell degeneration and visual field loss. Glaucoma is considered to be the leading cause of blindness in the industrialised countries. Oxidative damage is an important pathogenic factor in glaucoma, which triggers trabecular meshwork (TM) degeneration, which then leads to intraocular hypertension. Neurodegenerative insults during glaucomatous neurodegeneration initiate an immune response to restore tissue homeostasis. However, the oxidative stress (OS) that develops during the pathogenic processes of glaucoma, along with the agerelated OS, plays a critical role in shifting the physiological equilibrium. In the TM from glaucoma donors, proinflammatory markers were found, which were induced by the activation of a stress response. Chronic changes in the composition of antioxidants found in aqueous humour may induce alterations in TM as well as in the optic nerve head cells. Highlighting the pathogenic role of reactive oxygen species (ROS) in glaucoma has implications in preventing this disease. Various clinical trials are available to test the efficacy of antioxidant drugs in glaucoma management. In this review, we discuss the OS as a therapeutic target, suggesting that the modulation of a pro-oxidant/antioxidant status might be a relevant target for glaucoma prevention and therapy.