Role Of Reactive Oxygen Species Research Articles

Comparative analyses of RNA-seq and phytohormone data of sweetpotatoes inoculated with Dickeya dadantii causing bacterial stem and root rot of sweetpotato.

Bacterial stem and root rot (BSRR) in sweetpotato caused by Dickeya dadantii is one of the ten major diseases of sweetpotatoes in China. However, the molecular mechanism underlying the resistance of sweetpotato to D. dadantii remains unclear. This study adopted a resistance identification assay that conformed Guangshu87 (GS87) as BSRR-resistant and Xinxiang (XX) as susceptible. Compared to XX, GS87 effectively prevented the invasion and dissemination of D. dadantii in planta. An RNA sequencing (RNA-seq) analysis identified 54,844 expressed unigenes between GS87 and XX at four different stages. Further, it revealed that GS87 was more able to regulate the expressions of more unigenes after the inoculation with D. dadantii, including resistance (R) and transcription factors (TF) genes. Moreover, content measurements of disease resistance-related phytohormones showed that both jasmonic acids (JAs) and salicylic acids (SAs) accumulated in D. dadantii-inoculated sweetpotatoes, and JAs may negatively regulate sweetpotato resistance against D. dadantii and accumulated faster than SAs. Meanwhile, determinations of ROS production rate and relevant enzymatic/non-enzymatic activity highlighted the vital roles of reactive oxygen species (ROS) and superoxide dismutase (SOD) in confering GS87 resistance against D. dadantii. Additionally, several hub genes with high connectivity were highlighted through Protein-Protein interaction (PPI) network analysis. In summary, the findings in this study contribute to the understanding of the different responses of resistant and susceptible sweetpotato cultivars to D. dadantii infection, and it also provide the first insight into the relevant candidate genes and phytohormones involved in the resistance of sweetpotato to D. dadantii.

Exploring the Mechanism for the Photocatalytic Degradation of Oxytetracycline in Water using TiO2 and Supplementary Oxidants

The persistent presence of antibiotics in wastewater, exemplified by oxytetracycline (OTC), poses environmental risks, necessitating robust removal strategies. This study investigates the effectiveness of photocatalysis utilizing TiO2 (P25) treated at various temperatures, combined with different oxidants such as hydrogen peroxide (H2O2), potassium peroxydisulfate (PDS), potassium peroxomonosulfate (PMS) under diverse experimental conditions. The research systematically explores the impact of temperature, pH, and oxidant concentration on the efficiency of OTC degradation. Our findings reveal that the combination of P25/500, PDS, UV irradiation, and stirring demonstrates superior OTC degradation, surpassing 99% efficiency after 180 min. Optimal pH conditions are identified, emphasizing the importance of balancing acidity for enhanced performance. The study also provides insights into the optimal PDS concentration, indicating a threshold beyond which further increases yield diminishing returns. Mechanistic understanding is enhanced through scavenger experiments, elucidating the pivotal role of reactive oxygen species, particularly O2•−, in the photocatalytic process. This research offers a practical framework for TiO2-based photocatalysis in wastewater treatment, emphasizing tailored conditions for efficient antibiotic removal. The outcomes contribute valuable insights to the development of sustainable wastewater treatment protocols targeting antibiotic pollutants.

Reactive oxygen species in age-related musculoskeletal decline: implications for nutritional intervention.

Musculoskeletal disorders and age-related musculoskeletal decline are major contributors to the burden of ill health seen in older subjects. Despite this increased burden, these chronic disorders of old age receive a relatively small proportion of national research funds. Much has been learned about fundamental processes involved in ageing from basic science research and this is leading to identification of key pathways that mediate ageing which may help the search for interventions to reduce age-related musculoskeletal decline. This short review will focus on the role of reactive oxygen species in age-related skeletal muscle decline and on the implications of this work for potential nutritional interventions in sarcopenia. The key physiological role of reactive oxygen species is now known to be in mediating redox signalling in muscle and other tissues and ageing leads to disruption of such pathways. In muscle, this is reflected in an age-related attenuation of specific adaptations and responses to contractile activity that impacts the ability of skeletal muscle from ageing individuals to respond to exercise. These pathways provides potential targets for identification of logical interventions that may help maintain muscle mass and function during ageing.

Hypoxia-Induced Mitochondrial ROS and Function in Pulmonary Arterial Endothelial Cells.

Pulmonary artery endothelial cells (PAECs) are a major contributor to hypoxic pulmonary hypertension (PH) due to the possible roles of reactive oxygen species (ROS). However, the molecular mechanisms and functional roles of ROS in PAECs are not well established. In this study, we first used Amplex UltraRed reagent to assess hydrogen peroxide (H2O2) generation. The result indicated that hypoxic exposure resulted in a significant increase in Amplex UltraRed-derived fluorescence (i.e., H2O2 production) in human PAECs. To complement this result, we employed lucigenin as a probe to detect superoxide (O2-) production. Our assays showed that hypoxia largely increased O2- production. Hypoxia also enhanced H2O2 production in the mitochondria from PAECs. Using the genetically encoded H2O2 sensor HyPer, we further revealed the hypoxic ROS production in PAECs, which was fully blocked by the mitochondrial inhibitor rotenone or myxothiazol. Interestingly, hypoxia caused an increase in the migration of PAECs, determined by scratch wound assay. In contrast, nicotine, a major cigarette or e-cigarette component, had no effect. Moreover, hypoxia and nicotine co-exposure further increased migration. Transfection of lentiviral shRNAs specific for the mitochondrial Rieske iron-sulfur protein (RISP), which knocked down its expression and associated ROS generation, inhibited the hypoxic migration of PAECs. Hypoxia largely increased the proliferation of PAECs, determined using Ki67 staining and direct cell number accounting. Similarly, nicotine caused a large increase in proliferation. Moreover, hypoxia/nicotine co-exposure elicited a further increase in cell proliferation. RISP knockdown inhibited the proliferation of PAECs following hypoxia, nicotine exposure, and hypoxia/nicotine co-exposure. Taken together, our data demonstrate that hypoxia increases RISP-mediated mitochondrial ROS production, migration, and proliferation in human PAECs; nicotine has no effect on migration, increases proliferation, and promotes hypoxic proliferation; the effects of nicotine are largely mediated by RISP-dependent mitochondrial ROS signaling. Conceivably, PAECs may contribute to PH via the RISP-mediated mitochondrial ROS.

The ability in managing reactive oxygen species affects Escherichia coli persistence to ampicillin after nutrient shifts.

This research delves into the intriguing realm of bacterial persistence and its profound implications for biofilms, infections, and antibiotic efficacy. The study focuses on Escherichia coli and how the switch from different carbon sources to fatty acids influences the formation of persister-resilient bacterial cells resistant to antibiotics. The findings reveal a striking variation in survival rates, with a significant number of cells surviving ampicillin treatment after transitioning from glucose to oleic acid. The key revelation is the role of reactive oxygen species (ROS) in cell killing, particularly after switching from gluconeogenic carbons. The timing of ROS bursts aligns with the rapid killing phase, highlighting the critical impact of oxidative stress regulation on persistence frequency. This research provides valuable insights into bacterial persistence mechanisms, offering potential avenues for targeted therapeutic interventions to combat bacterial resistance effectively.

The Role of Reactive Oxygen Species from Heavy Metal: Effect on reactivity of Fish and Defensive Mechanism of Antibiotic Resistant Bacteria in Aquatic Environment

The Role of Reactive Oxygen Species from Heavy Metal: Effect on reactivity of Fish and Defensive Mechanism of Antibiotic Resistant Bacteria in Aquatic Environment

Light increases resistance of thylakoid membranes to thermal inactivation.

In the region of slightly acidic pH (рН 5.7), the manganese cluster in oxygen-evolving complex of photosystem II (PSII) is more resistant to exogenous reductants. The effect of such pH on the heat inactivation efficiency of the electron transport chain (O2 evolution and 2,6-dichlorophenolindophenol reduction) in PSII membranes and thylakoid membranes was investigated. Under thylakoid membranes illumination accompanied by lumen acidification, their resistance to heat inactivation increases. In the presence of protonophores, the rate of heat inactivation increases, which seems to be associated not with the protonophore mechanism, but with structural and/or functional changes in membranes. In PSII membrane preparations, the efficiency of the oxygen evolution inhibition at pH 5.7 is also lower than at pH 6.5. The role of reactive oxygen species in thermal inactivation of photosynthetic membranes was investigated using a lipophilic cyclic hydroxylamine ESR spin probe.

The Potential Role of Reactive Oxygen Species Produced by Low-Density Neutrophils in Periodontitis.

Neutrophils own an arsenal of dischargeable chemicals that enable them to handle bacterial challenges, manipulating innate immune response and actual participation in acquired immunity. The reactive oxygen species (ROS) are one of the most important chemicals that neutrophils discharge to eradicate pathogens. Despite their beneficial role, the ROS were strongly correlated to periodontal tissue destruction. Lowdensity neutrophils (LDN) have been recognized for producing enhanced quantities of ROS. However, the potential role of ROS produced by LDN in periodontitis is unknown. The aim of the study was to investigate the impact of ROS produced by LDN in periodontal diseases. Venous blood and periodontal parameters were obtained from 100 systemically healthy subjects divided into 40 participants with healthy periodontium in the control group and 60 with unstable periodontitis in the study group. Flow cytometry was used to measure the production of ROS by LDN in both groups. The data were analyzed for normal distribution using the Shapiro-Wilk test at p < 0.05, Spearman's correlations, and Mann-Whitney U test. Statistical analysis was performed in SPSS v25. No difference between the groups had been obtained in ROS production by LDN. However, a significant positive correlation existed between ROS and clinical attachment loss in periodontitis. LDN exhibits the same ROS generation capacity in the control and periodontitis groups.

Melatonin Treatment Alleviates Chilling Injury of Loquat Fruit via Modulating ROS Metabolism.

Cold storage is one of the most effective methods to maintain postharvest fruit quality. However, loquat fruits are prone to chilling injury (CI) during cold storage, appearing as symptoms such as browning and pitting, which leads to quality deterioration and economic losses. In this study, the effects of melatonin on CI alleviation and the potential role of reactive oxygen species (ROS) metabolism in loquat fruit were investigated. The results showed that 50 μM melatonin was the optimal concentration to inhibit the increase in CI index and cell membrane permeability. Moreover, compared to control fruits, 50 μM melatonin inhibited the malonaldehyde (MDA) content, O2-. production rate and H2O2 content (ROS accumulation) by 17.8%, 7.2% and 11.8%, respectively, during cold storage. Compared to non-treated loquats, 50 μM melatonin maintained higher levels of 1-diphenyl-2-picrylhydrazyl radical-scavenging ability and reducing power, as well as the contents of ascorbic acid (AsA) and glutathione (GSH). Additionally, 50 μM melatonin enhanced the activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) by increasing relevant gene expressions. The activities of SOD, CAT and APX were increased by up to 1.1-, 1.1- and 1.1-times (16 d) by melatonin, as compared with the control fruits. These findings indicate that melatonin mitigation of CI is involved in maintaining cellular redox apphomeostasis in loquat fruit during cold storage.

Exploring the Role of Reactive Oxygen Species in the Pathogenesis and Pathophysiology of Alzheimer's and Parkinson's Disease and the Efficacy of Antioxidant Treatment.

Alzheimer's (AD) and Parkinson's Disease (PD) are life-altering diseases that are characterised by progressive memory loss and motor dysfunction. The prevalence of AD and PD is predicted to continuously increase. Symptoms of AD and PD are primarily mediated by progressive neuron death and dysfunction in the hippocampus and substantia nigra. Central features that drive neurodegeneration are caspase activation, DNA fragmentation, lipid peroxidation, protein carbonylation, amyloid-β, and/or α-synuclein formation. Reactive oxygen species (ROS) increase these central features. Currently, there are limited therapeutic options targeting these mechanisms. Antioxidants reduce ROS levels by the induction of antioxidant proteins and direct neutralisation of ROS. This review aims to assess the effectiveness of antioxidants in reducing ROS and neurodegeneration. Antioxidants enhance major endogenous defences against ROS including superoxide dismutase, catalase, and glutathione. Direct neutralisation of ROS by antioxidants protects against ROS-induced cytotoxicity. The combination of Indirect and direct protective mechanisms prevents ROS-induced α-synuclein and/or amyloid-β formation. Antioxidants ameliorate ROS-mediated oxidative stress and subsequent deleterious downstream effects that promote apoptosis. As a result, downstream harmful events including neuron death, dysfunction, and protein aggregation are decreased. The protective effects of antioxidants in human models have yet to directly replicate the success seen in cell and animal models. However, the lack of diversity in antioxidants for clinical trials prevents a definitive answer if antioxidants are protective. Taken together, antioxidant treatment is a promising avenue in neurodegenerative disease therapy and subsequent clinical trials are needed to provide a definitive answer on the protective effects of antioxidants. No current treatment strategies have significant impact in treating advanced AD and PD, but new mimetics of endogenous mitochondrial antioxidant enzymes (Avasopasem Manganese, GC4419 AVA) may be a promising innovative option for decelerating neurodegenerative progress in the future at the mitochondrial level of OS.

Euphorbiaceae superoxide dismutase, catalase, and glutathione peroxidase as clues to better comprehend high drought tolerance in castor bean

Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPX) enzymes exert a central role in reactive oxygen species (ROS) scavenger in plants, being an important part of enzymatic antioxidant system. Despite the importance of these enzymes in ROS metabolism and in different signaling pathways related to plant development and stress response, their gene families have not yet been comprehensively characterized in many crop plants. Among different crops, the Euphorbiaceae family has some species highly tolerant to drought stress. However, the gene families that encode the antioxidant enzymes, as well as their role in this drought stress tolerance, remains not characterized. Here, the SOD, CAT, and GPX genes of castor bean (Ricinus communis), cassava (Manihot esculenta), jatropha (Jatropha curcas), rubber tree (Hevea brasiliensis), petty spurge (Euphorbia peplus), and annual mercury (Mercurialis annua) were identified and characterized. The comprehensive phylogenetic and genomic analyses allowed the classification of the genes into different classes and revealed the duplication events that contribute to the expansion of these families within plant genomes. The expression patterns of SOD, CAT, and GPX genes were examined in castor bean, cassava, jatropha, and rubber tree by RNA-seq analysis revealing differential expression during stress. Additionally, the castor bean gene expression was confirmed by RT-qPCR. Among castor bean genes, RcGPX4 appears to be induced in castor bean roots under drought stress, but the heterologous expression in Arabidopsis thaliana does not improve the drought tolerance. Altogether, this data has significantly contributed to characterizing the expression patterns and conducting evolutionary assessment of these genes in Euphorbiaceae. This bridge a gap in understanding the proposed functions of core components within the antioxidant mechanism in an economically significant group of plants, particularly during stress responses

Endurance exercise-induced histone methylation modification involved in skeletal muscle fiber type transition and mitochondrial biogenesis

Skeletal muscle is a highly heterogeneous tissue, and its contractile proteins are composed of different isoforms, forming various types of muscle fiber, each of which has its own metabolic characteristics. It has been demonstrated that endurance exercise induces the transition of muscle fibers from fast-twitch to slow-twitch muscle fiber type. Herein, we discover a novel epigenetic mechanism for muscle contractile property tightly coupled to its metabolic capacity during muscle fiber type transition with exercise training. Our results show that an 8-week endurance exercise induces histone methylation remodeling of PGC-1α and myosin heavy chain (MHC) isoforms in the rat gastrocnemius muscle, accompanied by increased mitochondrial biogenesis and an elevated ratio of slow-twitch to fast-twitch fibers. Furthermore, to verify the roles of reactive oxygen species (ROS) and AMPK in exercise-regulated epigenetic modifications and muscle fiber type transitions, mouse C2C12 myotubes were used. It was shown that rotenone activates ROS/AMPK pathway and histone methylation enzymes, which then promote mitochondrial biogenesis and MHC slow isoform expression. Mitoquinone (MitoQ) partially blocking rotenone-treated model confirms the role of ROS in coupling mitochondrial biogenesis with muscle fiber type. In conclusion, endurance exercise couples mitochondrial biogenesis with MHC slow isoform by remodeling histone methylation, which in turn promotes the transition of fast-twitch to slow-twitch muscle fibers. The ROS/AMPK pathway may be involved in the regulation of histone methylation enzymes by endurance exercise.

Photodegradation of tylosin tartrate by advanced oxidation processes.

Tylosin tartrate, a macrolide antibiotic, is one of a class of emerging contaminants that have been detected in natural bodies of water since they are not easily removed by conventional treatment processes. In this study, the direct and indirect photodegradation of tylosin tartrate was analyzed to understand the role of reactive oxygen species and organic matter that may be present in surface waters. While direct photolysis caused negligible degradation (k = (9.4 ± 1.8) × 10-5s-1), the addition of 0.4M hydrogen peroxide (k = (2.18 ± 0.01) × 10-4s-1) or usage of the photo-Fenton process (k = (2.96 ± 0.02) × 10-4s-1) resulted in greater degradation. The degradation was maximized by combining tylosin tartrate with an experimentally determined optimal concentration of humic acid (15mg/L), which readily produced singlet oxygen and increased the overall degradation (k = 1.31 ± 0.05) × 10-3s-1) by means of indirect photolysis. Absolute pseudo-first-order bimolecular reaction rate constants for tylosin tartrate were measured with singlet oxygen [(4.7936 ± 0.0001) × 105M-1s-1] and hydroxyl radical [(5.2693 ± 0.0002) × 109M-1s-1] using competition kinetics, and when combined with data on concentration of the reactive oxygen species, showed that the hydroxyl radical makes a contribution to the degradation that is approximately eleven orders of magnitude greater than singlet oxygen.

Oxidative Stress and Cataract Formation: Evaluating the Efficacy of Antioxidant Therapies.

This comprehensive review investigates the pivotal role of reactive oxygen species (ROS) in cataract formation and evaluates the potential of antioxidant therapies in mitigating this ocular condition. By elucidating the mechanisms of oxidative stress, the article examines how ROS contribute to the deterioration of lens proteins and lipids, leading to the characteristic aggregation, cross-linking, and light scattering observed in cataracts. The review provides a thorough assessment of various antioxidant strategies aimed at preventing and managing cataracts, such as dietary antioxidants (i.e., vitamins C and E, lutein, and zeaxanthin), as well as pharmacological agents with antioxidative properties. Furthermore, the article explores innovative therapeutic approaches, including gene therapy and nanotechnology-based delivery systems, designed to bolster antioxidant defenses in ocular tissues. Concluding with a critical analysis of current research, the review offers evidence-based recommendations for optimizing antioxidant therapies. The current literature on the use of antioxidant therapies to prevent cataract formation is sparse. There is a lack of evidence-based conclusions; further clinical studies are needed to endorse the use of antioxidant strategies in patients to prevent cataractogenesis. However, personalized treatment plans considering individual patient factors and disease stages can be applied. This article serves as a valuable resource, providing insights into the potential of antioxidants to alleviate the burden of cataracts.

Photolytic Mass Loss of Humic Substances Measured with a Quartz Crystal Microbalance.

Laboratory studies have shown that photolytic mass loss can be a significant sink for secondary organic aerosol (SOA). Here, we use a quartz crystal microbalance to measure mass loss of Suwannee River Humic Acid (SRHA) and Suwannee River Fulvic Acid (SRFA), surrogates for SOA, exposed to 254, 300, and 405 nm radiation over the course of 24 h. We find that the photolytic mass loss rates of these materials are comparable to those for laboratory-generated limonene and toluene SOA material from the study of Baboomian et al, ACS Earth Space Chem. 2020, 4, 1078. Scaling our results to ambient conditions, we estimate that humic substances in aerosols can lose as much as 8% by mass in the first day of exposure in the atmosphere, equivalent to 0.025% of J NO2 , the photolysis rate of nitrogen dioxide. By using zero air instead of nitrogen, we also find that the presence of oxygen accelerates the photolytic mass loss rate by a factor of 2 to 4 at all wavelengths suggesting a potential role for reactive oxygen species. UV photolysis of an aqueous SRFA solution demonstrated both photobleaching at UV wavelengths and photoenhancement at visible wavelengths. Ultrahigh-resolution mass spectrometric analysis showed that condensed-phase SRFA photolysis led to decreased intensity in the 100-300 m/z range while aqueous SRFA photolysis resulted in an increase in intensity in the same range. This work reaffirms that photolytic mass loss is a potentially significant sink for SOA, but only on the time scale of a day or two and demonstrates that SRHA and SRFA are suitable surrogates for atmospheric SOA with respect to photolytic mass loss.

Blocking Metallothionein-2 Expression by Copper-Doped Carbon Dots Induces Cellular Antioxidant System Collapse for Antitumor Therapy.

The insufficient antioxidant reserves in tumor cells play a critical role in reactive oxygen species (ROS)-mediated therapeutics. Metallothionein-2 (MT-2), an intracellular cysteine-rich protein renowned for its potent antioxidant properties, is intricately involved in tumor development and correlates with a poor prognosis. Consequently, MT-2 emerges as a promising target for tumor therapy. Herein, we present the development of copper-doped carbon dots (Cu-CDs) to target MT-2 to compromise the delicate antioxidant reserves in tumor cells. These Cu-CDs with high tumor accumulation and prolonged body retention can effectively suppress tumor growth by inducing oxidative stress. Transcriptome sequencing unveils a significant decrease in MT-2 expression within the in vivo tumor samples. Further mechanical investigations demonstrate that the antitumor effect of Cu-CDs is intricately linked to apolipoprotein E (ApoE)-mediated downregulation of MT-2 expression and the collapse of the antioxidant system. The robust antitumor efficacy of Cu-CDs provides invaluable insights into developing MT-2-targeted nanomedicine for cancer therapies.

Hyaluronic acid-coated porphyrin nanoplatform with oxygen sustained supplying and glutathione depletion for enhancing photodynamic/ion/chemo synergistic cancer treatment

Hypoxia and high concentration of glutathione (GSH) in tumor seriously hinder the role of reactive oxygen species (ROS) and oxygen-dependence strategy in tumor treatment. In this work, a self-generating oxygen and self-consuming GSH hyaluronic acid (HA)-coated porphyrin nanoplatform (TAPPP@CaO2/Pt(IV)/HA) is established for enhancing photodynamic/ion/chemo targeting synergistic therapy of tumor. During the efforts of ROS production by nanosystems, a GSH consuming strategy is implemented for augmenting ROS-induced oxidative damage for synergetic cancer therapy. CaO2 in the nanosystems is decomposed into O2 and H2O2 in an acidic environment, which alleviates hypoxia and enhances the photodynamic therapy (PDT) effect. Calcium overload causes mitochondria dysfunction and induces apoptosis. Pt (IV) reacts with GSH to produce Pt (II) for chemotherapy and reduce the concentration of GSH, protecting ROS from scavenging for augmenting ROS-induced oxidative damage. In vitro and in vivo results demonstrated the self-generating oxygen and self-consuming GSH strategy can enhance ROS-dependent PDT coupled with ion/chemo synergistic therapy. The proposed strategy not only solves the long-term problem that hypoxia limits therapeutic effect of PDT, but also ameliorates the highly reducing environment of tumors. Thus the preparation of TAPPP@CaO2/Pt(IV)/HA provided a novel strategy for the effective combined therapy of cancers.

The Effect of Carbon Nanotube Enantiomers in Macrophages

The inherent asymmetry within our bodies enables remarkable selectivity to chiral molecules. This selectivity is crucial because one stereoisomer may induce undesired effects, remain inactive, or, in the worst case, exhibit toxicity. Even though the knowledge of the interactions of stereoisomer, including enantiomer, with biological systems has been accumulated to a certain extent, our understanding of the body's response to single-wall carbon nanotube (SWCNT) enantiomers is very limited. In this study, we aimed to provide evidence of how macrophages respond to (6,5) enantiomers, finding the importance of their helicity at the nanometer scale. To achieve this, we first separated the left-handed (M) and right-handed (P) enantiomers of (6,5) using aqueous two-phase extraction (ATPE) and conducted a surfactant displacement procedure to coat them with single-stranded DNA. Following the separation and displacement processes, we quantified reactive oxygen species (ROS) as a crucial criterion for assessing the potential influence of the (6,5) enantiomers on macrophages. Considering ROS's role as a signaling molecule at a physiological level, quantifying ROS allows us to determine which enantiomer is more related to oxidative stress and, subsequently, nanotoxicity. To corroborate our findings, we conducted parallel assessments of cells, focusing on metabolic activity, cellular uptake, and proliferation. However, the complexity of the SWCNTs including the coating and aggregation states makes the observed cellular behaviors difficult to explain, even though the SWCNTs have been purified to the enantiomer level. In this regard, we probed the fluorescence signal to evaluate the aggregation states of SWCNTs, hoping to extract the sole enantiomer effects within biological environments. Our results improve the overall comprehension of the relation between SWCNT enantiomeric properties and macrophage responses, emphasizing the distinction between the left and right forms of SWCNTs and providing valuable insights for future biomedical applications of SWCNTs.

Overexpression of protection of telomeres 1 (POT1), a single-stranded DNA-binding proteins in alfalfa (Medicago sativa), enhances seed vigor

Extensive bodies of research are dedicated to the study of seed aging with a particular focus on the roles of reactive oxygen species (ROS), and the ensuing oxidative damage during storage, as a primary cause of seed vigor decreasing. ROS diffuse to the nucleus and damage the telomeres, resulting in a loss of genetic integrity. Protection of telomeres 1 (POT1) is a telomeric protein that binds to the telomere region, and plays an essential role in maintaining genomic stability in plants. In this study, there were totally four MsPOT1 genes obtained from alfalfa genome. Expression analysis of four MsPOT1 genes in germinated seed presented the different expressions. Four MsPOT1 genes displayed high expression levels at the early stage of seed germination, Among the four POT1 genes, it was found that MS. gene040108 was significantly up-regulated in the early germination stage of CK seeds, but down-regulated in aged seeds. RT-qPCR assays and RNA-seq data revealed that MsPOT1-X gene was significantly induced by seed aging treatment. Transgenic seeds overexpressing MsPOT1-X gene in Arabidopsis thaliana and Medicago trunctula exhibited enhanced seed vigor, telomere length, telomerase activity associated with reduced H2O2 content. These results would provide a new way to understand aging stress-responsive MsPOT1 genes for genetic improvement of seed vigor. Although a key gene regulating seed vigor was identified in this study, the specific mechanism of MsPOT1-X gene regulating seed vigor needs to be further explored.

Abstract Tu130: Intracellular Galectin-3 Interacts with Cytosolically Exposed Glycans to Promote the Injury of Cardiomyocytes Under Oxidative Stress

Background: Oxidative stress is a hallmark of cardiovascular (CV) diseases. The potential involvement of Galectin-3 (Gal-3) has been proposed in CV pathological conditions, but its role in reactive oxygen species (ROS)-induced cardiomyocyte damage remains elusive. Hypothesis: Oxidative stress leads to ruptures of membrane-bound organelles including lysosome. Intracellular Gal-3 of cardiomyocytes may interact with glycans exposed by ROS-damaged organelles to modulate downstream cellular signaling. Aims: To investigate whether intracellular Gal-3-glycan interactions may occur in ROS-treated cardiomyocytes and how such interactions may regulate cell survival or death. Methods and Results: Using cardiomyoblast H9c2 cells exposed to hydrogen peroxide (H 2 O 2 ) to be the cell model, we found that oxidative stress induced significant lysosomal damage followed by cell death. The immunofluorescence imaging showed that cytosolic Gal-3 aggregated into small puncta, which were colocalized with LAMP2. To examine whether the aggregation of Gal-3 was contributed by ROS-induced damage, catalase was ectopically expressed in H 2 O 2 -treated cells and the formation of Gal-3 puncta was attenuated. These results suggest that intracellular Gal-3 interacts with glycans presented by the ruptured lysosomes in H 2 O 2 -treated H9c2 cells, leading to puncta formation. To further delineate whether these Gal-3 puncta show a functional role in cell survival under oxidative stress, we knocked endogenous Gal-3 down in H9c2 cells by RNAi and found that Gal-3 ablation protected the cells from ROS-induced injuries. Moreover, the ectopic expression of N-terminally truncated Gal-3, which loses its protein-interaction function but preserved the carbohydrate-recognition ability, also prevented H9c2 cells from oxidative stress-caused damage. Conclusions: ROS-induced lysosomal rupture leads to intracellular Gal-3-glycan interactions, further recruiting cytosolic proteins and activating downstream cell death signaling cascades. Such intracellular Gal-3-glycan interactions may contribute to the cardiomyocyte injuries under oxidative stress.