Excess Oxygen Research Articles

Oxidative stress disrupts vascular microenvironmental homeostasis affecting the development of atherosclerosis.

Atherosclerosis is primarily an inflammatory reaction of the cardiovascular system caused by endothelial damage, leading to progressive thickening and hardening of the vessel walls, as well as extensive necrosis and fibrosis of the surrounding tissues, the most necessary pathological process causing cardiovascular disease. When the body responds to harmful internal and external stimuli, excess oxygen free radicals are produced causing oxidative stress to occur in cells and tissues. Simultaneously, the activation of inflammatory immunological processes is followed by an elevation in oxygen free radicals, which directly initiates the release of cytokines and chemokines, resulting in a detrimental cycle of vascular homeostasis abnormalities. Oxidative stress contributes to the harm inflicted upon vascular endothelial cells and the decrease in nitric oxide levels. Nitric oxide is crucial for maintaining vascular homeostasis and is implicated in the development of atherosclerosis. This study examines the influence of oxidative stress on the formation of atherosclerosis, which is facilitated by the vascular milieu. It also provides an overview of the pertinent targets and pharmaceutical approaches for treating this condition.

Inhibition of the FOXO1–ROCK1 axis mitigates cardiomyocyte injury under chronic hypoxia in Tetralogy of Fallot by maintaining mitochondrial quality control

IntroductionPersistent chronic myocardial hypoxia causes disturbances in mitochondrial quality control (MQC), ultimately leading to increased cardiomyocyte injury in patients with Tetralogy of Fallot (TOF). The present study aimed to identify the key effector molecules of cardiomyocyte injury under chronic hypoxia in TOF. MethodsClinical data from TOF patients were collected and whole transcriptome sequencing was performed on myocardial samples. Chronic hypoxia models were established in cardiac-specific knockout mice and cardiomyocytes, and a series of molecular experiments were used to determine the specific mechanisms involved. ResultsClinical cohort data and whole-transcriptome sequencing analysis of myocardial samples from TOF patients revealed that forkhead box O1 (FOXO1) plays an important role in chronic hypoxic cardiomyocyte injury. In a model of chronic hypoxia established in FOXO1 cardiac-specific knockout mice and FOXO1 gene-deficient cardiomyocytes, the AMPK signaling pathway regulates the expression of FOXO1, which in turn disrupts MQC by regulating the transcriptional activation of Rho-associated protein kinase 1 (ROCK1), and increasing the production of mitochondrial ROS, thereby exacerbating damage to cardiomyocytes. Excessive reactive oxygen species (ROS) production during MQC dysfunction further activates Cox7a2L to increase the assembly of the respiratory chain supercomplex. In addition, we found that miR-27b-3p partially binds to the 3′ untranslated region of FOXO1 to exert a protective effect. ConclusionsMaintenance of MQC under chronic hypoxia is achieved through a series of injury-protection mechanisms, suggesting that FOXO1 inhibition may be crucial for future mitigation of chronic hypoxic cardiomyocyte injury in TOF.

Stabilizing the Layer-Structured Oxide Cathode by Modulating the Oxygen Redox Activity for Sodium Ion Batteries.

The layer-structured oxide cathode for sodium-ion batteries has attracted a widespread attention due to the unique redox properties and the anionic redox activity providing additional capacity. Nevertheless, such excessive oxygen redox reactions will lead to irreversible oxygen release, resulting in a rapid deterioration of the cycling stability. Herein, sulfur ion is successfully introduced to the O3-NaNi0.3Mn0.5Cu0.1Ti0.05W0.05O2 material through high-temperature quenching, thereby developing a novel Na2S-modified O3/P2-NaNi0.3Mn0.5Cu0.1Ti0.05W0.05O2 composite with extended cycling life. The S2- is analyzed for the ability to enhance the reversibility of oxidation-reduction reactions under high voltage and suppress the loss of lattice oxygen during cycling. The stable S─O covalent bonds are found to inhibit the oxygen generation and release within the structure. Benefiting from these improvements, the Na₂S-modified O3/P2-NaNi0.3Mn0.5Cu0.1Ti0.05W0.05O2 exhibited a high reversible capacity of 173.1mA h g-1 over a wide voltage range of 1.5-4.3V under test conditions at 0.1 C and 81.5% capacity retention after 120 cycles at 1 C. The Na₂S-modified O3/P2-NaNi0.3Mn0.5Cu0.1Ti0.05W0.05O2 demonstrates the excellent rate capability with the reversible capacities of 173.1,137.0,114.7,96.7, and 80.1mA h g-1 at 0.1, 0.2, 0.5, 1, and 2 C.

Coupled digital visualization and multi-omics uncover neurobehavioral dysfunction in zebrafish induced by resorcinol bis(diphenylphosphate)

Resorcinol bis(diphenylphosphate) (RDP) is an emerging pollutant that has been frequently detected in aquatic environments, although its toxicity is poorly characterized. To understand how RDP affects the neural system, two-month-old zebrafish were exposed to RDP at concentrations of 0.1 and 10 μg/L for 60 days. Following exposure, behavioral assessments were conducted, revealing the emergence of anxiety-like symptoms and memory deficits among the adult fish exposed to RDP, especially at the higher concentration. The increased blood–brain barrier (BBB) permeability (4.67–5.58-fold higher than the control group), reduced expression of tight junction proteins and the rapid brain RDP bioaccumulation (15.63 ± 2.34 ng/g wet weight) indicated the neurotoxicity of RDP. Excess reactive oxygen species synthesis (2.20–2.50-fold) was induced by RDP, leading to mitochondrial dysfunction and decreased production of neurotransmitters in the brain, specifically serotonin (5-HT; 16.3 %) and dopamine (DA; 18.1 %). Metabolomic analysis revealed that the low-toxicity RDP dose up-regulated lipid-related metabolites, while the high-toxicity dose up-regulated arachidonic acid metabolism and disrupted amino acid metabolism, including tryptophan and tyrosine metabolism related to dopaminergic and serotonergic pathways. The dysregulation of genes in various cellular processes was identified by transcriptomics, mainly involved in cell adhesion molecules and gap junctions, and oxidative phosphorylation, which were directly associated with BBB permeability and oxidative stress, respectively. Correlation analysis of microbiome-metabolite-host links built a mechanistic hypothesis for alterations in gut microbiota (Actinobacteriota and Proteobacteria) induced by high-dose RDP leading to the alteration of tryptophan, tyrosine, and arachidonic acid metabolism, decreasing the production of 5-HT and DA through the gut-brain axis. This study provides valuable insights into the mechanism underlying RDP-induced neurotoxicity in zebrafish, which can inform ecological risk assessments.

Long-time oxidation resistance of KD-SiC fibers with different composition and structure in air atmosphere

Continuous silicon carbide (SiC) fibers, as reinforcement of ceramic matrix composites, have broad application prospects in the fields of aviation, aerospace and nuclear energy. Three typical KD-SiC fibers were adopted to explore the relationship of the composition and structure with their long-term oxidation (1–100 h) resistance in air environment. The mechanical strength retention of the nearly stoichiometric polycrystalline SiC fiber (C-1) was generally higher than that of the SiC fiber (C-3) with excess carbon and low oxygen, also higher than the nearly stoichiometric SiC fiber (C-2), especially under oxidation conditions of higher temperature and longer holding time. By comparing the high-temperature resistance with oxidation resistance at 1200–1600 °C, it was found that the oxidation reaction was the dominant factor affecting the mechanical properties. This work could provide theoretical and practical references for improvement of oxidation resistance of SiC fibers and their composites.

Nanozyme-enhanced injectable hyaluronic acid-based hydrogel for the treatment of osteoarthritis

The progression of osteoarthritis (OA) is dramatically accelerated by excessive reactive oxygen species (ROS)-induced apoptosis of chondrocytes and the inflammatory response of synovial macrophages. In this study, we developed an injectable hydrogel with a catalase-mimicking nanozyme activity as a therapeutic agent for OA. In vitro experiments confirmed that the HA and peroxide-mimetic nanoenzyme-enhanced hydrogel, containing ε-polylysine/Mn1.8Co1.2O4 (ε-PLE/MnCoO) nanoparticles, continuously eliminated ROS and inflammatory cytokines while promoting the polarization of inflammatory macrophages (M1 phenotype) towards anti-inflammatory macrophages (M2 phenotype) in dysfunctional microenvironments. When used for intraarticular injections in OA models, the nanoenzyme-enhanced hydrogel effectively reduced oxidative stress by scavenging ROS and regulating the immune microenvironment. It resulted in a subsequent reduction in the expression of inflammatory factors, including MMP-13, TNF-α, IL-1β, and iNOS in both the synovium and joint fluid. Moreover, cartilage repair was enhanced by the promotion of COL-2 and SOX-9 expression in the cartilage tissue, whereas osteophyte formation in OA was reduced. This study introduced an innovative treatment strategy for the clinical management of OA, demonstrating its significant potential for application in treating OA.

Inflammation-responsive PCL/gelatin microfiber scaffold with sustained nitric oxide generation and heparin release for blood-contacting implants

Delayed endothelialization, the excessive proliferation of smooth muscle cells (SMCs), and persistent inflammation are the main reasons for the implantation failure of blood-contacting materials. To overcome this problem, an inflammation-responsive, core-shell structured microfiber scaffold is developed using polycaprolactone (PCL), selenocystamine-modified gelatin (Gel-Se), L-ascorbyl 6-palmitate (AP), and dexamethasone as the fiber shell, with poly (l-lysine) (PLL) and heparin incorporated in the fiber core. Superhydrophilic microfiber scaffolds exhibit antifouling properties that inhibit protein adsorption and blood cell adhesion, thereby effectively mitigating the risk of acute thrombosis. The continuous release of heparin and sustained generation of nitric oxide (NO) through the catalytic decomposition of S-nitrosothiols by selenocystamine lead to a biomimetic endothelial function for the enhancement of blood compatibility. The inflammation-responsive compound AP can detoxify excess reactive oxygen species (ROS) while controlling the release of dexamethasone to reduce chronic inflammation. We demonstrate the ability of microfiber scaffolds to reduce thrombotic and inflammatory complications, inhibit SMC proliferation, and promote rapid endothelialization both in vitro and ex vivo. Hence, microfiber scaffolds are robust and promising for blood-contacting implants with enhanced antithrombogenicity and anti-inflammatory capabilities.

Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.

Humans have long been combating chronic pain. In clinical practice, opioids are firstchoice analgesics, but long-term use of these drugs can lead to serious adverse reactions. Finding new, safe and effective pain relievers that are useful treatments for chronic pain is an urgent medical need. Based on accumulating evidence from numerous studies, excess reactive oxygen species (ROS) contribute to the development and maintenance of chronic pain. Some antioxidants are potentially beneficial analgesics in the clinic, but ROS-dependent pathways are completely inhibited only by scavenging ROS directly targeting cellular or subcellular sites. Unfortunately, current antioxidant treatments do not achieve this effect. Furthermore, some antioxidants interfere with physiological redox signaling pathways and fail to reverse oxidative damage. Therefore, the key upstream processes and mechanisms of ROS production that lead to chronic pain in vivo must be identified to discover potential therapeutic targets related to the pathways that control ROS production in vivo. In this review, we summarize the sites and pathways involved in analgesia based on the three main mechanisms by which ROS are generated in vivo, discuss the preclinical evidence for the therapeutic potential of targeting these pathways in chronic pain, note the shortcomings of current research and highlight possible future research directions to provide new targets and evidence for the development of clinical analgesics.

Bioactive MXene hydrogel promotes structural and functional regeneration of skeletal muscle through improving autophagy and muscle innervation

Complete skeletal muscle regeneration after traumatic injuries remains a challenge due to impaired regenerative capability and dysregulated microenvironments. Autophagy plays a crucial role in the muscle regeneration process by regulating myogenic and non-myogenic cells. Herein, we report a bioactive MXene hydrogel (FPGM) capable of upregulating autophagy and increasing muscle innervation to restore skeletal muscle structure and function. FPGM possessed excellent electrical conductivity, tissue adhesive ability and antioxidation, which could eliminate excess reactive oxygen species to reduce oxidative stress and decrease the secretion of pro-inflammatory cytokine. FPGM upregulated the autophagy level of myoblasts and promoted the migration and tube formation of endothelial cells as well as myogenic differentiation with negligible toxicity. FPGM accelerated muscle fiber formation and skeletal muscle regeneration by improving autophagy, which could regulate microenvironment through raising M2 macrophages to alleviate excessive inflammation, facilitating angiogenesis and decreasing fibrous scar tissue formation in vivo. Importantly, FPGM could efficiently restore muscle function by improving muscle innervation, tibialis anterior compound muscle action potential amplitude and neuromuscular conduction. This work demonstrates that bioactive MXene hydrogel should be a promising candidate for complete skeletal muscle regeneration.

Perfluorooctanoic acid (PFOA) induces cardiotoxicity by activating the Keap1/Nrf2 pathway in zebrafish (Danio rerio) embryos

Perfluorooctanoic acid (PFOA), a perfluoroalkyl compound, is linked to congenital heart diseases, though its underlying mechanisms remain unclear. We hypothesized that PFOA induces cardiac defects through the inhibition of the Keap1/Nrf2 pathway, leading to oxidative damage in cardiomyocytes. In this study, zebrafish embryos exposed to PFOA showed significant cardiac malformations and dysfunction, characterized by excessive reactive oxygen species (ROS), malondialdehyde (MDA) production, decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. Additionally, we observed dysregulation in the expression of key cardiac development genes (vmhc, gata4, nkx2.5, and sox9b). PFOA also reduced the expression of keap1, nrf2, and ho-1. After overexpression of Nrf2, levels of ROS and MDA decreased, while levels of SOD, CAT, and GSH-Px increased. Additionally, cardiomyocyte apoptosis and cardiac malformations were alleviated. These findings have suggested that PFOA induces oxidative stress through Keap1/Nrf2 pathway inhibition, ultimately leading to cardiac defects.

Mitoquinone improves porcine embryo development through modulating oxidative stress and mitochondrial function

Oxidative stress caused by excess reactive oxygen species (ROS) is one of the main causes of low efficiency in in vitro production of embryos. These ROS can cause mitochondrial dysfunction and apoptosis, resulting in poor embryo development. Therefore, to prevent mitochondrial damage and apoptosis caused by ROS, we investigated the effects of mitoquinone (MitoQ), a mitochondrial-targeted antioxidant, on the in vitro culture (IVC) of porcine embryos. Various concentrations of MitoQ (0, 0.01, 0.1, or 1 nM) were supplemented during the entire period of IVC. The results showed that supplementation with 0.1 nM MitoQ significantly increased the blastocyst formation rate, with a higher total cell number including trophectoderm cell number and higher transcript expression of lineage-specific transcription factors in blastocysts. In addition, the 0.1 nM MitoQ-treated group showed a significantly lower percentage and number of apoptotic cells in blastocysts with positively regulated transcript expression of apoptosis-related genes. Therefore, 0.1 nM MitoQ was suggested as optimal concentration for porcine IVC and used for further investigations. MitoQ treatment significantly reduced intracellular ROS levels and increased glutathione levels in Day 2 embryos, with upregulated the transcript expression of antioxidant enzymes-related genes. Furthermore, the MitoQ group exhibited a significantly higher mitochondrial quantity, mitochondrial membrane potential, and ATP content in Day 2 embryos, with increased transcript expression of mitochondrial biogenesis-related genes. Taken together, these findings reveal that MitoQ supplementation can enhance the developmental competence of porcine embryos by decreasing oxidative stress and improving mitochondrial function.

Synergies of bioactivities, mechanisms, dietary factors and functional food applications of medicinal insulin plant (Costus pictus D.): a review

SummaryModernisation has significantly altered lifestyles, particularly eating habits, contributing to the increase of chronic diseases, with diabetes mellitus being a predominant metabolic disorder. Medicinal herbs such as Costus pictus (C. pictus), commonly known as the Insulin plant, offer a promising approach to managing these conditions. It is a perennial plant from the Costaceae family rich in proteins, fibres, minerals (K, Ca, Cr, Fe, Mn, Cu, Zn), and bioactive compounds. This review highlighted the plant's potential in mitigating chronic diseases and metabolic disorders due to its diverse bioactivities, including hepatoprotective, anti‐inflammatory, anticancer, antidiabetic, and antioxidant properties. These benefits are primarily attributed to its phytochemicals, mainly flavonoids and phenolic compounds. The antidiabetic mechanism involves suppressing metabolic enzymes essential for carbohydrate metabolism, while its antioxidant activity helps reduce excessive reactive oxygen species (ROS) levels implicated in various diseases. Furthermore, C. pictus can be incorporated into functional foods such as bakery and confectionery products, functional drinks, and edible coatings. We discussed the dietary factors, bioactivities, and underlying mechanisms associated with Costus pictus D., emphasising its applicability in functional food formulations. The synthesis of current research highlights the plant's role in modulating glucose metabolism, enhancing antioxidant defences, and its potential in mitigating diseases such as diabetes. By delving into the synergies between its dietary factors and bioactivities, this review aims to elucidate the multifaceted benefits of Costus pictus D., thereby fostering its integration into sustainable agricultural practises and contributing to public health nutrition.

Two Distinct Charge Orders in Infinite-Layer PrNiO2+δ Revealed by Resonant X-Ray Diffraction

Abstract Research of infinite-layer nickelates has unveiled a broken translation symmetry, which has sparked significant interest in its root, its relationship to superconductivity, and its comparison to charge order in cuprates. In this study, resonant x-ray scattering measurements were performed on thin films of infinite-layer PrNiO2+δ . The results show significant differences in the superlattice reflection at the Ni L 3 absorption edge compared to that at the Pr M 5 resonance in their dependence on energy, temperature, and local symmetry. These differences point to two distinct charge orders, although they share the same in-plane wavevectors. It is suggested that these dissimilarities could be linked to the excess oxygen dopants, given that the resonant reflections were observed in an incompletely reduced PrNiO2+δ film. Furthermore, azimuthal analysis indicates that the oxygen ligands likely play a crucial role in the charge modulation revealed at the Ni L 3 resonance.

Durable electrocatalysts based on barium niobates doped with Ca, Fe, and Y: Enhancing catalytic activity and selectivity for oxidative coupling of methane

Effective conversion of methane into value added products such as olefins, is a major research area for the past 40 years. Electrochemical oxidative coupling of methane (E-OCM) is recently gaining attention due to its ability to control the product selectivity by oxide ion flux and applied potential. We report a new series of catalysts, Ca, Fe, and Y co-doped barium niobate perovskites (BCNFY) for E-OCM application. BCNFY perovskites show chemical stability under 4 % H2, CH4, and high CH4-O2 mixtures at high temperatures up to 900 °C. Under reducing conditions, BCNFY perovskites form excess oxygen vacancies that is supported by Nb4+/5+ oxidation state changes that help retain the crystal structure. Temperature programmed reaction (TPR) measurements under 95 % CH4:5% O2 reveal methane activation properties from 600 °C with a high C2+ selectivity of 82 % at 850 °C. TPR measurements further reveal the nature of active sites for methane activation. Cyclic voltammetry measurements show a unique relationship between product selectivity and applied potential as at applied biases close to open circuit potential, CO and H2 are the major products while at high applied biases ethylene and CO2 are the major products. Our results show the advantages of E-OCM over conventional OCM although improvements in terms of electronic conductivity of the electrode and overall current densities are required for commercial viability for these perovskite electrodes.

Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets

The human brain is highly dependent on oxygen, utilizing approximately 20% of the body’s oxygen at rest. Oxygen deprivation to the brain can lead to loss of consciousness within seconds and death within minutes. Recent studies have identified regions of the brain with spontaneous episodic hypoxia, referred to as “hypoxic pockets”. Hypoxia can also result from impaired blood flow due to conditions such as heart disease, blood clots, stroke, or hemorrhage, as well as from reduced oxygen intake or excessive oxygen consumption caused by factors like low ambient oxygen, pulmonary diseases, infections, inflammation, and cancer. Severe hypoxia in the brain can manifest symptoms similar to Parkinson’s disease (PD), including cerebral edema, mood disturbances, and cognitive impairments. Additionally, the development of PD appears to be closely associated with hypoxia and hypoxic pathways. This review seeks to investigate the molecular interactions between hypoxia and PD, emphasizing the pathological role of hypoxic pathways in PD and exploring their potential as therapeutic targets.

Determination of beneficial effects of cuminaldehyde on hyperglycemiaassociated kidney malfunctions.

Type 1 diabetes mellitus is defined by the autoimmune destruction of pancreatic β cells, with diabetic nephropathy being a significant consequence. Recently, cuminaldehyde has been shown protective ability against various pathophysiology. However, its nephroprotective and anti-diabetic potential has not yet been fully understood. We, therefore, conducted the present study to evaluate the anti-hyperglycemic potential of cuminaldehyde in NRK52E cells without (control) or with high glucose medium to emulate hyperglycemic conditions. Cuminaldehyde pre-treatment at an optimal concentration of 175μM prior to high glucose addition restricted excessive reactive oxygen species (ROS) production and maintained cellular morphology to almost normal. The inhibitor study using N-acetyl-l-cysteine confirmed that blocking of ROS assists NRK52E cells in evading apoptosis. In addition, hyperglycemia was induced in 6-week-old Swiss albino mice in this investigation through the intraperitoneal injection of streptozotocin (150mgkg-1 body weight). Hyperglycemia increased the kidney-to-body weight ratio, lowered serum insulin levels, and led to significant renal tissue damage compared to control mice. Moreover, hyperglycemia disturbs cellular redox equilibrium by decreasing antioxidant enzyme functions and promoting inflammatory cytokines in kidney tissue. Administering cuminaldehyde at a dosage of 10mgkg-1 body weight for 5weeks daily after the onset of diabetes effectively ameliorated the aforementioned anomalies and reversed kidney damage by regulating inflammation-induced cell death. Overall, the research demonstrated that cuminaldehyde has hypoglycemic, antioxidant, anti-inflammatory, and anti-apoptotic properties. We believe that after conducting extensive research, this unique molecule can be used in clinical trials against diabetic nephropathy in future.

Enhanced Stability Under Positive Bias Temperature Stress in Oxide Thin Film Transistors with Double Gate Structure By Improving Bottom Channel Interface

In this paper, we discuss the causes of reliability degradation in oxide TFTs with a double gate structure and propose methods for improvement. Reducing IGZO deposition power significantly improves PBTS (Positive Bias Temperature Stability) reliability in double gate structures. This improvement is attributed to reduction of excess oxygen defects accumulated at the bottom channel interface, as inferred from the difference in PBTS results for the top single gate and double gate structures

Using Hybrid MnO2-Au Nanoflowers to Accelerate ROS Scavenging and Wound Healing in Diabetes

Objectives: Excessive reactive oxygen species (ROS) in diabetic wounds are major contributors to chronic wounds and impaired healing, posing significant challenges in regenerative medicine. Developing innovative drug delivery systems is crucial to address these issues by modifying the adverse microenvironment and promoting effective wound healing. Methods: Herein, we designed a novel drug delivery platform using manganese dioxide nanoflower hybridized gold nanoparticle composites (MnO2-Au) synthesized via a hydrothermal reaction, and investigated the potential of MnO2-Au nanoflowers to relieve the high oxidative stress microenvironment and regulate diabetic wound tissue healing. Results: This hybrid material demonstrated superior catalytic activity compared to MnO2 alone, enabling the rapid decomposition of hydrogen peroxide and a substantial reduction in ROS levels within dermal fibroblasts. The MnO2-Au nanoflowers also facilitated enhanced dermal fibroblast migration and Col-I expression, which are critical for tissue regeneration. Additionally, a hydrogel-based wound dressing incorporating MnO2-Au nanoflowers was developed, showing its potential as an intelligent drug delivery system. This dressing significantly reduced oxidative stress, accelerated wound closure, and improved the quality of neonatal epithelial tissue regeneration in a diabetic rat skin defect model. Conclusions: Our findings underscore the potential of MnO2-Au nanoflower-based drug delivery systems as a promising therapeutic approach for chronic wound healing, particularly in regenerative medicine.

The transcription factor RppA regulates chlorophyll and carotenoid biosynthesis to improve photoprotection in cyanobacteria.

Chlorophyll is an essential photosynthetic pigment but also a strong photosensitizer. Excessive free chlorophyll and its precursors can cause oxidative damage to photosynthetic organisms. Cyanobacteria are the oldest oxygenic photosynthetic organisms and the ancestors of the chloroplast. Owing to their complex habitats, cyanobacteria require precise regulation of chlorophyll synthesis to respond to environmental factors, especially changes in light. Chlorophyll synthase, encoded by chlG, is the enzyme catalyzing the final step of chlorophyll biosynthesis, which is closely related to photosynthesis biogenesis. However, the transcriptional regulation on chlG remains unclear. Here, the transcription factor, regulator of photosynthesis and photopigment-related gene expression A (RppA) was identified to bind to the chlG promoter by screening a yeast one-hybrid library in the cyanobacterium Synechocystis sp. PCC 6803. The rppA knock-out mutant showed a phenotype of slow growth and severe oxidative damage under dark-light transition conditions. The up-regulated transcriptional expression of chlG was significantly higher and more chlorophyll and its precursors accumulated in the rppA knock-out mutant than those in the wild-type strain during the transition from darkness to light, indicating RppA represses the expression of chlG in Synechocystis. Meanwhile, RppA could synchronously promote the transcription of carotenoids biosynthesis-related genes to enhance carotenoids synthesis during the dark-light transition. These results reveal synergistic regulation of chlorophyll and carotenoids biosynthesis in cyanobacteria in response to frequent dark-light transitions, which slows down chlorophyll biosynthesis while promoting carotenoids biosynthesis to avoid oxidative damage caused by excessive reactive oxygen species accumulation.

Iridium Single-Atom-Ensembles Stabilized on Mn-Substituted Spinel Oxide for Durable Acidic Water Electrolysis.

Exploring single-atom-catalysts for the acidic oxygen evolution reaction (OER) is of paramount importance for cost-effective hydrogen production via acidic water electrolyzers. However, the limited durability of most single-atom-catalysts and Ir/Ru-based oxides under harsh acidic OER conditions, primarily attributed to excessive lattice oxygen participation resulting in metal-leaching and structural collapse, hinders their practical application. Herein, an innovative strategy is developed to fabricate short-range Ir single-atom-ensembles (IrSAE) stabilized on the surface of Mn-substituted spinel Co3O4 (IrSAE-CMO), which exhibits excellent mass activity and significantly improved durability (degradation-rate: ≈2mVh-1), outperforming benchmark IrO2 (≈44mVh-1) and conventional Irsingle-atoms on pristine-Co3O4 for acidic OER. First-principle calculations reveal that Mn-substitution in the octahedral sites of Co3O4 substantially reduces the migration energy barrier for Irsingle-atoms on the CMO surface compared to pristine-Co3O4, facilitating the migration of Irsingle-atoms to form strongly correlated IrSAE during pyrolysis. Extensive ex situ characterization, operando X-ray absorption and Raman spectroscopies, pH-dependence activity tests, and theoretical calculations indicate that the rigid IrSAE with appropriate Ir-Ir distance stabilized on the CMO surface effectively suppresses lattice oxygen participation while promoting direct O─O radical coupling, thereby mitigating Ir-dissolution and structural collapse, boosting the stability in an acidic environment.