Role Of Reactive Oxygen Species Research Articles

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.

Persulfidation of plant and bacteroid proteins is involved in legume nodule development and senescence.

Legumes establish symbiosis with rhizobia, forming nitrogen-fixing nodules. The central role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in nodule biology has been clearly established. Recently, hydrogen sulfide (H2S) and other reactive sulfur species (RSS) have emerged as novel signaling molecules in animals and plants. A major mechanism by which ROS, RNS, and RSS fulfil their signaling role is the post-translational modification of proteins. To identify possible functions of H2S in nodule development and senescence, we used the tag-switch method to quantify changes in the persulfidation profile of common bean (Phaseolus vulgaris) nodules at different developmental stages. Proteomic analyses indicate that persulfidation plays a regulatory role in plant and bacteroid metabolism and senescence. The effect of a H2S donor on nodule functioning and on several proteins involved in ROS and RNS homeostasis was also investigated. Our results using recombinant proteins and nodulated plants support a crosstalk among H2S, ROS, and RNS, a protective function of persulfidation on redox-sensitive enzymes, and a beneficial effect of H2S on symbiotic nitrogen fixation. We conclude that the general decrease of persulfidation levels observed in plant proteins of aging nodules is one of the mechanisms that disrupt redox homeostasis leading to senescence.

Peculiarities of the morpho-physiological reactions of mosses depending on the water-temperature regime of their local growth

The morphological structure of and the activity of the catalase of mosses Ptychostomum imbricatulum and Brachythecium rutabulum depending on microclimatic conditions of their local growth were studied. The morphological variability of moss turfs in different ecological conditions of forest ecosystems was established, in particular, the influence of the level of moisture in local growth on the morphometric parameters of mosses (the density of the turf, the height of the shoots and their foliage and the size of the leaves) was revealed. It is shown that the morphological structure of the turfs of the mosses Ptychostomum imbricatulum and Brachythecium rutabulum is important for moisture conservation and depends on the microclimatic conditions of local growth and the life form of the species. It is shown that the increase in the content of hydrogen peroxide as a signaling mediator is a component of the antioxidant protection system. It was established that the highest content of hydrogen peroxide was in shoots of P. imbricatulum from the territory of pine plantations, where the microclimatic conditions are the least favorable. The obtained results indicate the existence of interdependence between the formation of reactive oxygen species and the activity of catalase as one of the key enzymes of antioxidant protection, which indicates the signaling role of reactive oxygen species in moss cells under stress conditions. The dependence of catalase activity in moss cells on the level of hydration of their turfs was established. The activation of catalase in adverse water and temperature conditions in the shoots of the studied species indicates the participation of the enzyme in the adaptation of plants to stress and is due to the strengthening of free radical oxidation processes, in particular, an increase in the content of hydrogen peroxide.

Exploring the potential impact of herbal antioxidants on human cardiovascular diseases

The body's antioxidant system efficiently neutralizes reactive oxygen species, which are intermediates formed during routine metabolic activity. Oxidative stress resulting from an imbalance in this neutralization process is known to be a key factor in many human ailments, including atherosclerosis and various cardiovascular diseases. Observational epidemiological research conducted over the past several decades has shown that consumption of vegetables and fruits rich in vitamins and antioxidants is associated with a reduced incidence of cardiovascular disease. However, it is crucial to exercise caution when considering the use of herbal antioxidants as a treatment for various ailments, including cardiovascular conditions. This caution arises from concerns related to their safety, potentially life-threatening side effects, toxicity, and potential interactions with other medications. Multiple research studies have highlighted these risks associated with antioxidant usage as a form of medical intervention. This overview briefly summarizes cardiovascular disease, associated risk factors, and the role of reactive oxygen species and oxidative stress in its development. Next, delve into some of the most significant plant-based antioxidants, their therapeutic uses, as well as the potential benefits and drawbacks of using them to treat various diseases, with a particular focus on their relevance to cardiovascular disease.

Role of reactive oxygen species in age-related disruption of mitochondrial networks in skeletal muscle and cartilage

Role of reactive oxygen species in age-related disruption of mitochondrial networks in skeletal muscle and cartilage

ROS Modulate Cell Death Mechanism in Cervical Cancer Cells Treated with the Combination of Polyphenolic Compounds and Anticancer Drug Cisplatin: A Review

Background: Most cervical cancer fatalities have been reported due to drug resistance, invasion, and metastasis. Combination therapy is a prominent technique for overcoming the toxicity of cancer chemotherapy to normal cells, which is mediated across numerous targeted pathways and requires a lower dose of each individual agent. Polyphenolic substances have the potential to improve chemotherapy efficacy while also reducing negative effects. Aims: This study aimed to review the research findings on the role of reactive oxygen species (ROS) in cervical cancer cell HeLa treated with combination therapy. Results: Hydroxyl radicals damage DNA, causing a cascade of structural changes in purine and pyrimidine bases that could lead to mutagenicity. ROS, such as hydroxyl radical (OH-), superoxide anions (O2 -), hydrogen peroxide (H2O2), and peroxyl radicals (ROO-), are frequent products of aerobic metabolism that can be beneficial or detrimental to the biological system. To combat the harmful effects of ROS, cells have an antioxidative defense system that comprises superoxide dismutases, catalase, glutathione, and other defensive mechanisms. Excessive ROS accumulation causes DNA damage, which triggers the apoptotic machinery, resulting in cell death. Conclusion: Chemotherapeutic medications with phenolic compounds or polyphenol-rich extracts exhibit anticancer synergy. Combination treatment with polyphenols and anticancer drugs is one of the promising approaches in the treatment of cervical cancer.

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

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

GROWTH RESPONSES OF PLANTS UNDER WATER STRESS: INVOLVEMENT OF REACTIVE OXYGEN SPECIES (ROS)

Plant growth is a vulnerable process being affected by several factors under natural conditions. All types of stresses encountered in natural environment affect plant growth and ultimately reduce productivity of crop plants. Recent global climatic changes made the situation more serious by causing problems like water deficit, high salinity, heat stress and different diseases caused by fungi, pest or bacteria as fallout. Water stress is considered as one of the major abiotic stress factors that limit plant growth and ultimately reduces the productivity of crop plants up to 80% of total production. A huge amount of land of our country is suffering from poor irrigation or irregular rainfall. Such problem calls for a demand for water use efficient or water resistant varieties of crop plants. To develop water resistant varieties, it is important to understand the growth mechanism of crop plants under water limited condition. Keeping in view of these problems this review work is focused light to the understanding of the role of Reactive Oxygen Species (ROS) in growth responses of plant under normal as well as water stress condition.

Identification of immune-related gene signatures for chronic obstructive pulmonary disease with metabolic syndrome: evidence from integrated bulk and single-cell RNA sequencing data.

Chronic obstructive pulmonary disease (COPD) is closely related to innate and adaptive inflammatory immune responses. It is increasingly becoming evident that metabolic syndrome (MetS) affects a significant portion of COPD patients. Through this investigation, we identify shared immune-related candidate biological markers. The Weighted Gene Co-Expression Network Analysis (WGCNA) was utilized to reveal the co-expression modules linked to COPD and MetS. The commonly expressed genes in the COPD and MetS were utilized to conduct an enrichment analysis. We adopted machine-learning to screen and validate hub genes. We also assessed the relationship between hub genes and immune cell infiltration in COPD and MetS, respectively. Moreover, associations across hub genes and metabolic pathways were also explored. Finally, we chose a single-cell RNA sequencing (scRNA-seq) dataset to investigate the hub genes and shared mechanisms at the level of the cells. We also applied cell trajectory analysis and cell-cell communication analysis to focus on the vital immune cell we were interested in. As a result, we selected and validated 13 shared hub genes for COPD and MetS. The enrichment analysis and immune infiltration analysis illustrated strong associations between hub genes and immunology. Additionally, we applied metabolic pathway enrichment analysis, indicating the significant role of reactive oxygen species (ROS) in COPD with MetS. Through scRNA-seq analysis, we found that ROS might accumulate the most in the alveolar macrophages. In conclusion, the 13 hub genes related to the immune response and metabolism may serve as diagnostic biomarkers and treatment targets of COPD with MetS.

Tetracycline removal via three-way synergy between pistachio shell powder, zerovalent copper or iron, and peroxymonosulfate activation

Pistachio shell powder (PS) immobilized zerovalent iron and zerovalent copper (ZVI@PS and ZVC@PS) were investigated for the tetracycline (TCH) removal via sulfate radical based advanced oxidation process (S-AOP's). Eco-efficient ZVI@PS and ZVC@PS nanocomposite prepared by one-pot redox precipitation method were characterized by using FTIR, XRD, SEM, BET, TGA/DTA, and XPS techniques. The EDX, TGA, and AAS analysis techniques confirmed the loading of 44 % Fe and 40 % Cu (w/w %) onto the pistachio shell biomass in ZVI@PS and ZVC@PS nanocomposites, respectively. This report comprehensively discusses the effect of various contributing factors for the TCH removal via advanced oxidation processes such as catalytic dosage, initial pH, PMS dosage and initial TCH concentrations, etc. Besides that, the role of reactive oxygen species (SO4−,.OH, O2−, and 1O2) in the TCH degradation process was investigated using radical scavenging experiments. A three-way synergistic approach was established between adsorption efficiencies of pistachio shell powder, heterogeneous ZVI or ZVC mediated Fenton-process and enhanced PMS activation process, for the observed enhanced TCH degradations. The observed rate constant (kobs.) values of ZVI@PS-PMS (0.34 min−1) and ZVC@PS-PMS (0.16 min−1) processes for TCH removal suggests that the ZVI@PS was more efficient in TCH removal compared to ZVC@PS.

Role of reactive oxygen species and antioxidative enzymes in the loss and re-establishment of desiccation tolerance in germinated pea seeds

This study highlights the regulatory function of ROS and its detoxifying enzymes during the loss and re-establishment of desiccation tolerance (DT) in PEG pretreated and untreated germinated pea (Pisum sativum L.) seeds with 2 mm long radicles. Dehydration of untreated pea seedlings to initial water content (IWC; 0.11 gH2O g−1 DM) and below IWC (0.06 gH2O g−1 DM) reduced the DT to 60 and 20 %, respectively. Significant amelioration in DT was observed in PEG pretreated seedlings by ∼100 % and 70 % following dehydration at IWC and below IWC, respectively. Rendering DT in the PEG pretreated seedlings was negatively associated with an extensive reduction in superoxide (∼2.3 folds) and H2O2 (∼1.8 folds) levels compared to the untreated seedlings. Enhanced expression, levels (quantitative) and number (isoenzyme) of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) in the PEG pretreated seedlings negatively correlated with the lowering ROS levels and its associated oxidative damage. It is concluded that the re-induction of increased antioxidative capacity is a key factor in the re-establishment of DT in PEG-pretreated pea seedlings. Additionally, PEG pretreatment resulted in 50 % disappearance of superoxide in the sub-apical zone (SZ) of the radicle compared to the radicle of untreated seedlings dehydrated below IWC. Further, in situ detection of superoxide accumulation in the apical zone (AZ) was NADPH-oxidase dependent but in the SZ it was independent of NADPH-oxidase. Our results showed that the osmotic stress induced the expression of antioxidative enzymes in germinated pea seeds and made them desiccation tolerant against oxidative stress caused by desiccation/drought.

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration.

Increased production and buildup of reactive oxygen species (ROS) can lead to various health issues, including metabolic problems, cancers, and neurological conditions. Our bodies counteract ROS with biological antioxidants such as SOD, CAT, and GPx, which help prevent cellular damage. However, if there is an imbalance between ROS and these antioxidants, it can result in oxidative stress. This can cause genetic and epigenetic changes at the molecular level. This review delves into how ROS plays a role in disorders caused by oxidative stress. We also look at animal models used for researching ROS pathways. This study offers insights into the mechanism, pathology, epigenetic changes, and animal models to assist in drug development and disease understanding.

Nimbolide Inhibits SOD2 to Control Pancreatic Ductal Adenocarcinoma Growth and Metastasis.

Reactive oxygen species are frequently associated with various cancers including pancreatic ductal adenocarcinomas (PDACs). Superoxide dismutase 2 (SOD2) is an enzyme that plays an important role in reactive oxygen species (ROS) signaling. Investigating the molecular function and biological functions of SOD2 can help us develop new therapeutic options and uncover new biomarkers for PDAC diagnosis and prognosis. Here, we show that nimbolide (NB), a triterpene limonoid, effectively blocks the growth and metastasis of PDACs by suppressing the expression and activity of SOD2. To identify the role of SOD2 in NB-induced anticancer activity, we used RNA interference to silence and plasmid transfection to overexpress it. Silencing SOD2 significantly reduced the growth and metastatic characteristics like epithelial-to-mesenchymal transition, invasion, migration, and colony-forming capabilities of PDACs, and NB treatment further reduced these characteristics. Conversely, the overexpression of SOD2 enhanced these metastatic characteristics. ROS signaling has a strong feedback mechanism with the PI3K/Akt signaling pathway, which could be mediated through SOD2. Finally, NB treatment to SOD2-overexpressing PDAC xenografts resulted in significant inhibition of tumor growth and metastasis. Overall, this work suggests that NB, a natural and safe phytochemical that silences SOD2 to induce high levels of ROS generation, results in increased apoptosis and reduced growth and progression of PDACs. The role of SOD2 in regulating NB-induced ROS generation presents itself as a therapeutic option for PDACs.