Reactive Oxygen Species Degradation Research Articles

Tweaking the NRF2 signaling cascade in human myelogenous leukemia cells by artificial nano-organelles

NRF2 (nuclear factor erythroid-2-related factor 2) is a key regulator of genes involved in the cell's protective response to oxidative stress. Upon activation by disturbed redox homeostasis, NRF2 promotes the expression of metabolic enzymes to eliminate reactive oxygen species (ROS). Cell internalization of peroxisome-like artificial organelles that harbor redox-regulating enzymes was previously shown to reduce ROS-induced stress and thus cell death. However, if and to which extent ROS degradation by such nanocompartments interferes with redox signaling pathways is largely unknown. Here, we advance the design of H2O2-degrading artificial nano-organelles (AnOs) that exposed surface-attached cell penetrating peptides (CPP) for enhanced uptake and were equipped with a fluorescent moiety for rapid visualization within cells. To investigate how such AnOs integrate in cellular redox signaling, we engineered leukemic K562 cells that report on NRF2 activation by increased mCherry expression. Once internalized, ROS-metabolizing AnOs dampen intracellular NRF2 signaling upon oxidative injury by degrading H2O2. Moreover, intracellular AnOs conferred protection against ROSinduced cell death in conditions when endogenous ROS-protection mechanisms have been compromised by depletion of glutathione or knockdown of NRF2. We demonstrate CPP-facilitated AnO uptake and AnO-mediated protection against ROS insults also in the T lymphocyte population of primary peripheral blood mononuclear cells from healthy donors. Overall, our data suggest that intracellular AnOs alleviated cellular stress by the on-site reduction of ROS.

Arginine with leucine drives reactive oxygen species-mediated integrin α5β1 expression and promotes implantation in mouse blastocysts.

The implantation rate of in vitro fertilization (IVF)-derived blastocysts after embryo transfer remains low, suggesting that the inadequate expression of specific proteins in culture-induced IVF-derived blastocysts contributes to low implantation rates. Therefore, treatment with appropriate regulation may improve the blastocyst implantation ability. This study demonstrated that the combination of l-arginine (Arg) and l-leucine (Leu) exerts distinct effects on IVF-derived mouse blastocysts. Arg with Leu promotes blastocyst implantation, whereas Arg alone decreases the blastocyst ability. Integrin α5β1 expression was increased in blastocysts treated with Arg and Leu. Arg with Leu also increased reactive oxygen species (ROS) levels and showed a positive correlation with integrin α5β1. Ascorbic acid, an antioxidant, decreased ROS and integrin α5β1 levels, which were elevated by Arg with Leu. Meanwhile, the mitochondrial membrane potential (ΔΨm) in blastocysts did not differ between treatments. Glutathione peroxidase (GPx) is involved in ROS scavenging using glutathione (GSH) as a reductant. Arg with Leu decreased GPx4 and GSH levels in blastocysts, and blastocysts with higher ROS levels had lower GPx4 and GSH levels. In contrast, Arg alone increased the percentage of caspase-positive cells, indicating that Arg alone, which attenuated implantation ability, was associated with apoptosis. This study revealed that elevated ROS levels induced by Arg with Leu stimulated integrin α5β1 expression, thereby enhancing implantation capacity. Our results also suggest that ROS were not due to increased production by oxidative phosphorylation, but rather to a reduction in ROS degradation due to diminished GPx4 and GSH levels.

Potassium and jasmonic acid —Induced nitrogen and sulfur metabolisms improve resilience against arsenate toxicity in tomato seedlings

Despite the well-known individual roles of potassium (K+) and jasmonic acid (JA) in plant responses to various stresses, their combined effects on improving tolerance to metalloid arsenate (AsV) toxicity and their influence on physiological and biochemical mechanisms remain largely unexplored. Therefore, the present study was conducted to explore the concomitant role of K+ and JA in nitrogen (N) and sulfur (S) metabolisms and regulation of antioxidant system in tomato seedlings under AsV toxicity conditions. The obtained data reveal that K+ and/or JA boosted the tolerance of tomato (Solanum lycopersicum L.) seedlings to AsV toxicity. However, the effect of a combined dose of K+ and JA was found to be more efficient as compared to the alone application. Seedlings subjected to AsV exhibited suppressed morphological attributes (shoot and root length, shoot and root fresh weight, and shoot and root dry weight), and physio-biochemical characteristics. Also, AsV-treated tomato seedlings showed enhanced reactive oxygen species (ROS) and increased the activity of ROS-producing enzymes (O2•— -generating NADPH oxidase activity and H2O2-generating glycolate oxidase] and also a chlorophyll (Chl) degrading enzyme [chlorophyllase (Chlase) activity]. However, the exogenous supply of K+ and JA synergistically inhibited Chl degradation and overproduction of ROS by suppressing their responsible enzymes activity. Moreover, it induced gas exchange parameters and activity of enzymes responsible for the photosynthesis process (carbonic anhydrase and Rubisco), Chl biosynthesis (δ-aminolevulinic acid dehydratase), and suppressed Chlase activity, and overproduction of ROS and their producing enzymes activity. Most interestingly, the combined application of K+ and JA substantially increased N and S content and their assimilation by upregulating the activity of enzymes involved in these key pathways (nitrate reductase, nitrite reductase, glutamine synthetase, glutamate synthase, ATP sulfurylase, adenosine 5-phosphosulfate reductase, O-acetylserine (thiol) lyase and sulfide reductase). The obtained results strongly reveal that the combined application of K+ and JA improved tolerance of tomato seedlings to AsV toxicity by enhancing N and S assimilation pathways and antioxidant system.

Mesoporous Ternary Nanozymes with Anti‐Senescence and Anti‐Inflammation Activities for Atherosclerosis Management

AbstractNumerous anti‐inflammatory agents and corresponding therapeutic strategies have been explored for treating inflammation‐related atherosclerosis, which has struggled with compromised antiatherosclerotic efficacy due to the complex pathogenesis. The senescent endothelial cells participate fundamentally at all stages in atherosclerosis, providing the basis for developing senotherapies to blunt the deleterious effects of senescent cells. In this work, a mesoporous palladium‐boron‐phosphorus ternary nanozyme with intrinsic superoxide dismutase/catalase‐mimicking properties is rationally engineered to co‐load H2 (an anti‐inflammatory agent) within nanozyme's crystal lattice and 4,4′‐dimethoxychalcone (DIM, an anti‐senescence agent) within mesopores, which elicits strong anti‐inflammatory effect in pro‐inflammatory macrophages by elimination of reactive oxygen species (ROS), H2 anti‐inflammation and promotion of cholesterol efflux, while simultaneously exerts anti‐senescence capacity in endothelial cells by protection of DNA from ROS damage and degradation of the cellular senescent components via autophagy activation. Both in vitro and in vivo experimental results verify the synergy between nanozyme‐based anti‐inflammatory therapy and autophagy activation, demonstrating that such a precise regulation of vascular senescence is applicable to augment antiatherosclerotic efficiency, which provides the nanomedicine‐enabled and senotherapy‐based paradigm for atherosclerosis management.

The CsAP2-09-CsWRKY25-CsRBOH2 cascade confers resistance against citrus bacterial canker by regulating ROS homeostasis.

Citrus bacterial canker (CBC) is a serious bacterial disease caused by Xanthomonas citri subsp. citri (Xcc) that adversely impacts the global citrus industry. In a previous study, we demonstrated that overexpression of an Xcc-inducible apetala 2/ethylene response factor encoded by Citrus sinensis, CsAP2-09, enhances CBC resistance. The mechanism responsible for this effect, however, is not known. In the present study, we showed that CsAP2-09 targeted the promoter of the Xcc-inducible WRKY transcription factor coding gene CsWRKY25 directly, activating its transcription. CsWRKY25 was found to localize to the nucleus and to activate transcriptional activity. Plants overexpressing CsWRKY25 were more resistant to CBC and showed higher expression of the respiratory burst oxidase homolog (RBOH) CsRBOH2, in addition to exhibiting increased RBOH activity. Transient overexpression assays in citrus confirmed that CsWRKY25 and CsRBOH2 participated in the generation of reactive oxygen species (ROS) bursts, which were able to restore the ROS degradation caused by CsAP2-09 knockdown. Moreover, CsWRKY25 was found to bind directly to W-box elements within the CsRBOH2 promoter. Notably, CsRBOH2 knockdown had been reported previously to reduce the CBC resistance, while demonstrated in this study, CsRBOH2 transient overexpression can enhance the CBC resistance. Overall, our results outline a pathway through which CsAP2-09-CsWRKY25 transcriptionally reprograms CsRBOH2-mediated ROS homeostasis in a manner conducive to CBC resistance. These data offer new insight into the mechanisms and regulatory pathways through which CsAP2-09 regulates CBC resistance, highlighting its potential utility as a target for the breeding of CBC-resistant citrus varieties.

Mechanism of interaction between ascorbic acid and soil iron-containing minerals for peroxydisulfate activation and organophosphorus flame retardant degradation

Soil constituents may play an important role in peroxydisulfate (PDS)-based oxidation of organic contaminants in soil. Iron-containing minerals (Fe-minerals) have been found to promote PDS activation for organics degradation. Our study found that ascorbic acid (H2A) could enhance PDS activation by soil Fe-minerals for triphenyl phosphate (TPHP) degradation. Determination and characterization analyses of Fe fractions showed that H2A could induce the reductive dissolution of solid Fe-minerals and the increasing of oxygen vacancies/hydroxyl groups content on Fe-minerals surface. The increasing of divalent Fe (Fe(II)) accelerated PDS activation to generate reactive oxygen species (ROS). Electron paramagnetic resonance (EPR) and quenching studies showed that sulfate radicals (SO4•−) and hydroxyl radicals (HO•) contributed significantly to TPHP degradation. The composition and content of Fe-minerals and soil organic matter (SOM) markedly influenced ROS transformations. Surface-bond and structural Fe played the main role in the production of Fe(II) in reaction system. The high-concentration SOM could result in ROS consumption and degradation inhibition. Density functional theory (DFT) studies revealed that H2A is preferentially adsorbed at α-Fe2O3(012) surface through Fe–O–C bridges rather than hydrogen bonds. After absorption, H atoms on H2A may further be migrated to adjacent O atoms on the α-Fe2O3(012) surface. With the transformation of H atoms to the α-Fe2O3(012) surface, the Fe–O–C bridge is broken and one electron is transferred from the O to Fe atom, inducing the reduction of trivalent Fe (Fe(III)) atom. MS/MS2 analysis, HPLC analysis, and toxicity assessment demonstrated that TPHP was transformed to less toxic 4-hydroxyphenyl diphenyl phosphate (OH-TPHP), diphenyl hydrogen phosphate (DPHP), and phenyl phosphate (PHP) through phenol-cleavage and hydroxylation processes, and even be mineralized in reaction system.

Genome-Wide Investigation and Expression Analysis of the Catalase Gene Family in Oat Plants (Avena sativa L.).

Through the degradation of reactive oxygen species (ROS), different antioxidant enzymes, such as catalase (CAT), defend organisms against oxidative stress. These enzymes are crucial to numerous biological functions, like plant development and defense against several biotic and abiotic stresses. However, despite the major economic importance of Avena sativa around the globe, little is known about the CAT gene's structure and organization in this crop. Thus, a genome-wide investigation of the CAT gene family in oat plants has been carried out to characterize the potential roles of those genes under different stressors. Bioinformatic approaches were used in this study to predict the AvCAT gene's structure, secondary and tertiary protein structures, physicochemical properties, phylogenetic tree, and expression profiling under diverse developmental and biological conditions. A local Saudi oat variety (AlShinen) was used in this work. Here, ten AvCAT genes that belong to three groups (Groups I-III) were identified. All identified CATs harbor the two conserved domains (pfam00199 and pfam06628), a heme-binding domain, and a catalase activity motif. Moreover, identified AvCAT proteins were located in different compartments in the cell, such as the peroxisome, mitochondrion, and cytoplasm. By analyzing their promoters, different cis-elements were identified as being related to plant development, maturation, and response to different environmental stresses. Gene expression analysis revealed that three different AvCAT genes belonging to three different subgroups showed noticeable modifications in response to various stresses, such as mannitol, salt, and ABA. As far as we know, this is the first report describing the genome-wide analysis of the oat catalase gene family, and these data will help further study the roles of catalase genes during stress responses, leading to crop improvement.

Kuwanon H Inhibits Melanoma Growth through Cytotoxic Endoplasmic Reticulum Stress and Impaired Autophagy Flux.

Although great progress has been made recently in targeted and immune-based therapies, additional treatments are needed for most melanoma patients due to acquired chemoresistance, recurrence, or metastasis. Elevated autophagy is required for the pathogenesis of melanoma to attenuate metabolic stress, protecting cancer cells from chemotherapeutics or radiation. Thus, intervention with autophagy is a promising strategy for melanoma treatment. Here, we examined a novel antimelanoma natural compound named kuwanon H (KuH), which significantly inhibited melanoma cell growth in vitro/vivo. Mechanistically, KuH induced cytotoxic endoplasmic reticulum (ER) stress, which inhibited cell viability and induced apoptosis. Meanwhile, KuH-induced ER stress mediated autophagysome formation through the ATF4-DDIT3-TRIB3-AKT-MTOR axis. Importantly, KuH impaired autophagy flux, which contributed to the anticancer effects of KuH. Finally, our results showed that KuH enhanced the sensitivity of melanoma cells to cisplatin, both in vitro and in vivo, by impairing autophagy degradation of reactive oxygen species and damaged mitochondria. Our findings indicate that KuH is a promising candidate anticancer natural product for melanoma therapy.

A Theory of Mechanical Stress-Induced H2O2 Signaling Waveforms in Planta

Recent progress in nanotechnology-enabled sensors that can be placed inside of living plants has shown that it is possible to relay and record real-time chemical signaling stimulated by various abiotic and biotic stresses. The mathematical form of the resulting local reactive oxygen species (ROS) wave released upon mechanical perturbation of plant leaves appears to be conserved across a large number of species, and produces a distinct waveform from other stresses including light, heat and pathogen-associated molecular pattern (PAMP)-induced stresses. Herein, we develop a quantitative theory of the local ROS signaling waveform resulting from mechanical stress in planta. We show that nonlinear, autocatalytic production and Fickian diffusion of H2O2 followed by first order decay well describes the spatial and temporal properties of the waveform. The reaction-diffusion system is analyzed in terms of a new approximate solution that we introduce for such problems based on a single term logistic function ansatz. The theory is able to describe experimental ROS waveforms and degradation dynamics such that species-dependent dimensionless wave velocities are revealed, corresponding to subtle changes in higher moments of the waveform through an apparently conserved signaling mechanism overall. This theory has utility in potentially decoding other stress signaling waveforms for light, heat and PAMP-induced stresses that are similarly under investigation. The approximate solution may also find use in applied agricultural sensing, facilitating the connection between measured waveform and plant physiology.

A Series of Ni Complexes Based on a Versatile ATCUN-Like Tripeptide Scaffold to Decipher Key Parameters for Superoxide Dismutase Activity.

The cellular level of reactive oxygen species (ROS) has to be controlled to avoid some pathologies, especially those linked to oxidative stress. One strategy for designing antioxidants consists of modeling natural enzymes involved in ROS degradation. Among them, nickel superoxide dismutase (NiSOD) catalyzes the dismutation of the superoxide radical anion, O2•-, into O2 and H2O2. We report here Ni complexes with tripeptides derived from the amino-terminal CuII- and NiII-binding (ATCUN) motif that mimics some structural features found in the active site of the NiSOD. A series of six mononuclear NiII complexes were investigated in water at physiological pH with different first coordination spheres, from compounds with a N3S to N2S2 set, and also complexes that are in equilibrium between the N-coordination (N3S) and S-coordination (N2S2). They were fully characterized by a combination of spectroscopic techniques, including 1H NMR, UV-vis, circular dichroism, and X-ray absorption spectroscopy, together with theoretical calculations and their redox properties studied by cyclic voltammetry. They all display SOD-like activity, with a kcat ranging between 0.5 and 2.0 × 106 M-1 s-1. The complexes in which the two coordination modes are in equilibrium are the most efficient, suggesting a beneficial effect of a nearby proton relay.

Thermally enhanced biodegradation of benzo[a]pyrene and benzene co-contaminated soil: Bioavailability and generation of ROS

In this study, a set of comprehensive experiments were conducted to explore the effects of temperature on the biodegradation, bioavailability, and generation of reactive oxygen species (ROS) by thermally enhanced biodegradation (TEB) under benzene and BaP co-contaminated conditions. The biodegradation rates of benzene increased from 57.4% to 88.7% and 84.9%, and the biodegradation efficiency of BaP was enhanced from 15.8% to 34.6% and 28.6%, when the temperature was raised from the ambient temperature of 15 °C to 45 °C and 30 °C, respectively. In addition, the bioavailability analysis results demonstrated that the water- and butanol-extractable BaP increased with elevated temperatures. High enzymatic activities and PAH-RHDα gene in gram-positive bacteria favored the long-term elevated temperatures (30 and 45 °C) compared to gram-negative bacteria. Moreover, ROS species (O2•− and •OH) generation was detected which were scavenged by the increased superoxide dismutase and catalase activities at elevated temperatures. Soil properties (pH, TOC, moisture, total iron, Fe3+, and Fe2+) were affected by the temperature treatments, revealing that metal-organic-associated reactions occurred during the TEB of benzene–BaP co-contamination. The results concluded that biodegradation of benzene–BaP co-contamination was greatly improved at 45 °C and that microbial activities enhanced the biodegradation under TEB via the increased bioavailability and generation and degradation of ROS.

ANAC087 transcription factor positively regulates age-dependent leaf senescence through modulating the expression of multiple target genes in Arabidopsis.

Leaf senescence is the final stage of leaf development and appropriate onset and progression of leaf senescence are critical for reproductive success and fitness. Although great progress has been made in identifying key genes regulating leaf senescence and elucidating the underlining mechanisms in the model plant Arabidopsis, there is still a gap to understanding the complex regulatory network. In this study, we discovered that Arabidopsis ANAC087 transcription factor (TF) positively modulated leaf senescence. Expression of ANAC087 was induced in senescing leaves and the encoded protein acted as a transcriptional activator. Both constitutive and inducible overexpression lines of ANAC087 showed earlier senescence than control plants, whereas T-DNA insertion mutation and dominant repression of the ANAC087 delayed senescence rate. A quantitative reverse transcription-polymerase chain reaction (qRT-PCR) profiling showed that the expression of an array of senescence-associated genes was upregulated in inducible ANAC087 overexpression plants including BFN1, NYE1, CEP1, RbohD, SAG13, SAG15, and VPEs, which are involved in programmed cell death (PCD), chlorophyll degradation and reactive oxygen species (ROS) accumulation. In addition, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) assays demonstrated that ANAC087 directly bound to the canonical NAC recognition sequence (NACRS) motif in promoters of its target genes. Moreover, mutation of two representative target genes, BFN1 or NYE1 alleviated the senescence rate of ANAC087-overexpression plants, suggesting their genetic regulatory relationship. Taken together, this study indicates that ANAC087 serves as an important regulator linking PCD, ROS, and chlorophyll degradation to leaf senescence.

Gallic Acid Accelerates the Oxidation Ability of the Peracetic Acid/Fe(III) System for Bisphenol A Removal: Fate of Various Radicals

Conveniently and cost-effectively obtained Fe(III) can be utilized for peracetic acid (PAA) activation in the presence of natural polyphenols. However, the effect of polyphenols on the fate of generated reactive oxygen species (ROS) remains unclear. In this study, it was demonstrated that Fe(III) can efficiently trigger PAA oxidation of pollutants with the assistance of gallic acid (GA), a widely distributed natural polyphenol. The GA/Fe(III)/PAA system efficiently removed bisphenol A (BPA) over a wide initial pH range of 4.0–7.0, with a removal rate of >90% over 20 min. Further, •OH played a dominant role in BPA degradation, and O2•– functioned as an intermediate contributing to the partial generation of •OH. The generated organic radicals (R-O•) did not considerably contribute to BPA removal. Apart from GA itself, both the reaction intermediates (phenoxy radicals) of GA with ROS and BPA degradation intermediates were crucial for the regeneration of Fe(II) from Fe(III) and the subsequent enhanced activation of PAA. Notably, further comprehensive analysis revealed an increase in •OH yield, but a decrease in R-O• production as the dosage of GA was increased from 10 to 100 μM. This finding emphasized the importance of properly utilizing GA, considering the reactivity of varied ROS toward different contaminants. R-O• (CH3CO2• and CH3CO3•) was quickly consumed by the GA-Fe(II) complex through single-electron transfer (SET) and/or by GA via H-abstraction (HAA). This study proposes a promising strategy for improving the Fe(III)/PAA process and advances the understanding of the trade-off between radical generation and elimination by polyphenols in PAA-based advanced oxidation processes (AOPs).

Uniform titania-supported Ce(iii) carbonate cluster catalysts for degradation of reactive oxygen species.

We report the synthesis of uniform 2.5 ± 0.4 nm diameter Ce(iii) carbonate clusters deposited on the surface of TiO2 nanoparticles and characterize them using HAADF-STEM and EELS, as well as UV-Vis and FTIR spectroscopies. This material is a highly proficient catalytic antioxidant for the degradation of photocatalytically generated reactive oxygen species (ROS). We observed an unusual U-shaped pH-dependence in its photoprotection catalytic activity, with an optimum function in the near-neutral pH range of 7.7 ± 0.7. This sharp pH dependence is not observed in previously reported bulk Ce(iii) carbonate materials, and it is also not a consequence of Ce(iii) carbonate cluster decomposition. However, it is consistent with a tandem reaction sequence consisting of a biomimetic superoxide dismutase and catalase function, which is dependent on a balance of protons and hydroxide anions for function. Our dissolution-deposition approach for synthesizing nanoscale Ce(iii) carbonate clusters on TiO2 should be generalizable to other carbonates and metal-oxide supports.

A theory of mechanical stress-induced H2O2 signaling waveforms in Planta

Recent progress in nanotechnology-enabled sensors that can be placed inside of living plants has shown that it is possible to relay and record real-time chemical signaling stimulated by various abiotic and biotic stresses. The mathematical form of the resulting local reactive oxygen species (ROS) wave released upon mechanical perturbation of plant leaves appears to be conserved across a large number of species, and produces a distinct waveform from other stresses including light, heat and pathogen-associated molecular pattern (PAMP)-induced stresses. Herein, we develop a quantitative theory of the local ROS signaling waveform resulting from mechanical stress in planta. We show that nonlinear, autocatalytic production and Fickian diffusion of H2O2 followed by first order decay well describes the spatial and temporal properties of the waveform. The reaction-diffusion system is analyzed in terms of a new approximate solution that we introduce for such problems based on a single term logistic function ansatz. The theory is able to describe experimental ROS waveforms and degradation dynamics such that species-dependent dimensionless wave velocities are revealed, corresponding to subtle changes in higher moments of the waveform through an apparently conserved signaling mechanism overall. This theory has utility in potentially decoding other stress signaling waveforms for light, heat and PAMP-induced stresses that are similarly under investigation. The approximate solution may also find use in applied agricultural sensing, facilitating the connection between measured waveform and plant physiology.

Role of Oxidative Stress and Antioxidants in Acquired Inner Ear Disorders.

Oxygen metabolism in the mitochondria is essential for biological activity, and reactive oxygen species (ROS) are produced simultaneously in the cell. Once an imbalance between ROS production and degradation (oxidative stress) occurs, cells are damaged. Sensory organs, especially those for hearing, are constantly exposed during daily life. Therefore, almost all mammalian species are liable to hearing loss depending on their environment. In the auditory pathway, hair cells, spiral ganglion cells, and the stria vascularis, where mitochondria are abundant, are the main targets of ROS. Excessive generation of ROS in auditory sensory organs is widely known to cause sensorineural hearing loss, and mitochondria-targeted antioxidants are candidates for treatment. This review focuses on the relationship between acquired hearing loss and antioxidant use to provide an overview of novel antioxidants, namely medicines, supplemental nutrients, and natural foods, based on clinical, animal, and cultured-cell studies.

Effects of Hypoxia on Coral Photobiology and Oxidative Stress.

Simple SummaryWith the growing importance of climate change research, the biological effects of oxygen loss on marine biota remain understudied. Coral reefs support diverse marine organisms and provide valuable ecosystem services. Deoxygenation may induce mass coral mortality and reduce species richness on coral reefs. Corals exposed to nocturnal hypoxia may experience detrimental effects due to induced oxidative stress caused by the increase in reactive oxygen species (ROS). The stress interferes with the most fundamental biological processes vital for the symbiosis between corals and photosynthetic algae. In this study, the coral Acropora spp. exhibited evident injury in photosynthetic apparatus, de-epoxidation state and DNA. However, besides that, there were no signs of engaged antioxidant defense mechanisms against ROS or pigment degradation, which leads to a conclusion that these corals may be resilient to such oxygen daily oscillations. Nevertheless, while corals might survive such short-term abiotic stress, the growing number and intensity of hypoxic events across the global ocean may pose a massive threat to these keystone invertebrate species.Global ocean oxygen (O2) content is decreasing as climate change drives declines in oxygen solubility, strengthened stratification of seawater masses, increased biological oxygen consumption and coastal eutrophication. Studies on the biological effects of nocturnal decreased oxygen concentrations (hypoxia) on coral reefs are very scarce. Coral reefs are fundamental for supporting one quarter of all marine species and essential for around 275 million people worldwide. This study investigates acute physiological and photobiological responses of a scleractinian coral (Acropora spp.) to overnight hypoxic conditions (<2 mg/L of O2). Bleaching was not detected, and visual and physical aspects of corals remained unchanged under hypoxic conditions. Most photobiological-related parameters also did not show significant changes between treatments. In addition to this, no significant differences between treatments were observed in the pigment composition. However, hypoxic conditions induced a significant decrease in coral de-epoxidation state of the xanthophyll cycle pigments and increase in DNA damage. Although the present findings suggest that Acropora spp. is resilient to some extent to short-term daily oxygen oscillations, long-term exposure to hypoxia, as predicted to occur with climate change, may still have deleterious effects on corals.

Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms.

BackgroundAbdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPARα) agonist, on AAA formation and rupture.MethodsExperimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in ApoE–/– mice for 4 weeks. Pemafibrate (0.1 mg/kg/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS).ResultsThe size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-α in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPARα significantly attenuated the anti-oxidative effect of pemafibrate.ConclusionPemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells.

Histological, metabolomic and transcriptomic analyses reveal mechanisms of cold acclimation of the Moso bamboo (Phyllostachys edulis) leaf.

The Moso bamboo (Phyllostachys edulis) leaf copes well with cold winters in southeastern China. However, until now, there has been almost no research on its adaptation mechanisms to cold weather. Herein, we found that the Moso bamboo leaf has evolved several anatomical structures that may play a role in enhancing its cold tolerance. These structures include fewer fusiform cells, smaller bulliform cells, lower stomata density and many more trichomes, as well as lower relative water content than in the leaf of a cold-sensitive bamboo species, Bambusa ventricosa. Untargeted metabolomic analysis revealed that the winter leaf of Moso bamboo had 10- to 1000-fold higher stress-resistant metabolites such as glutathione, trehalose and ascorbic acid than the leaf of B. ventricosa on both warm and cold days. In contrast to the leaves that grew on a warm day, some metabolites such as glutathione and trehalose increased dramatically in the leaves of Moso bamboo that grew on a cold day. However, they unexpectedly decreased in the leaf of B. ventricosa growing at cold temperatures. Transcriptome analysis revealed a cold stress response network that includes trehalose, glutathione, flavonoid metabolism, DNA repair, reactive oxygen species degradation, stress-associated genes and abiotic stress-related plant hormones such as jasmonic acid, abscisic acid and ethylene. The potential mediator transcription factors, such as EREBP, HSF, MYB, NAC and WRYK, were also significantly upregulated in Moso bamboo leaves growing at cold temperatures. Interestingly, many newly identified genes were involved in the transcriptome of the winter leaf of the Moso bamboo. Most of these new genes have not even been annotated yet. The above results indicate that the Moso bamboo leaf has evolved special histological structures, metabolic pathways and a cold stress-tolerant transcriptome to adapt to the cold weather in its distribution areas.

Metabolic Pathway of Natural Antioxidants, Antioxidant Enzymes and ROS Providence.

Based on the origin, we can classify different types of stress. Environmental factors, such as high light intensity, adverse temperature, drought, or soil salinity, are summarized as abiotic stresses and discriminated from biotic stresses that are exerted by pathogens and herbivores, for instance. It was an unexpected observation that overproduction of reactive oxygen species (ROS) is a common response to all kinds of stress investigated so far. With respect to applied aspects in agriculture and crop breeding, this observation allows using ROS production as a measure to rank the stress perception of individual plants. ROS are important messengers in cell signaling, but exceeding a concentration threshold causes damage. This requires fine-tuning of ROS production and degradation rates. In general, there are two options to control cellular ROS levels, (I) ROS scavenging at the expense of antioxidant consumption and (II) enzyme-controlled degradation of ROS. As antioxidants are limited in quantity, the first strategy only allows temporarily buffering of a certain cellular ROS level. This way, it prevents spells of eventually damaging ROS concentrations. In this review, we focus on the second strategy. We discuss how enzyme-controlled degradation of ROS integrates into plant metabolism. Enzyme activities can be continuously operative. Cellular homeostasis can be achieved by regulation of respective gene expression and subsequent regulation of the enzyme activities. A better understanding of this interplay allows for identifying traits for stress tolerance breeding of crops. As a side effect, the result also may be used to identify cultivation methods modifying crop metabolism, thus resulting in special crop quality.