Cellular H2O2 Research Articles

Hydrogen peroxide pretreatment assisted phytoremediation of sodium dodecyl sulfate by Juncus acutus L

BackgroundSodium Dodecyl Sulfate (SDS) an anionic surfactant pollutant has emerged as a serious hazard to the aquatic and terrestrial environment. Due to physical and chemical methodological difficulties for SDS removal, phytoremediation techniques are efficient alternative strategies to tackle such adversities. Juncus acutus L. (J. acutus) is a pioneer wetland species that has been recently exploited for phytoremediation purposes. To our knowledge, the role of exogenous hydrogen peroxide (H2O2), in improving the phytoextraction of SDS has not been examined yet. In this study, pretreatment foliar spray of H2O2 (15 mM) combined with two levels of SDS (50 and 100 ppm) in water culture was evaluated to remove SDS contamination and add value to the phytoremediation process.ResultsThe outcomes revealed that J. acutus has considerable translocation and bioaccumulation abilities for SDS and can be utilized as an appropriate hyperaccumulator in SDS-contaminated sites. However, the involvement of H2O2 extended phytoremediation capacity and successive removal of SDS. H2O2 significantly assisted in increasing SDS remediation via more accumulation in J. acutus tissues by 29.9 and 112.4% and decreasing SDS concentration in culture media by 33.3 and 27.3% at 50 and 100 ppm SDS, respectively. Bioaccumulation factor (BCF) increased by 13.8 and 13.2%, while translocation factor (TCF) positively maximized by 82.4 and 76.2% by H2O2 application at 50 and 100 ppm SDS, respectively. H2O2 pretreatment could drive the decline in biochemical attributes in SDS-affected plants by modulating stress tolerance indices, pigments, water relations, proline content, enzymatic activities, and further, reduced oxidative stress in terms of electrolyte leakage, cellular H2O2, malondialdehyde (MDA) accumulation.ConclusionsH2O2 could play a potential role in maximizing phytoremediation capacity of SDS by J. acutus in polluted sites.

Manganese-functionalized MXene theranostic nanoplatform for MRI-guided synergetic photothermal/chemodynamic therapy of cancer

Abstract Two-dimensional transition metal carbides and nitrides (MXenes) nanosheets with high photothermal conversion efficiency as well as photothermal stability can efficiently generate remarkable hyperthermia for photothermal therapy (PTT) of cancer. However, mono-MXenes cannot exhibit precise diagnosis and treatment to complete ablation of cancer cells in the PTT process. To overcome this dilemma, an “all-in-one” nanoplatform of titanium carbide (Ti3C2) MXene-based composite nanosheets is developed for magnetic resonance imaging (MRI)-guided multi-modal hyperthermia and chemodynamic tumor ablation, which was achieved by bonding of manganese ion on the surface of Ti3C2, and then was the functionalized nanosheets was modified by biocompatible PEG (Mn-Ti3C2@PEG). Due to magnetic and Fenton-like catalytic properties of Mn components, Mn-Ti3C2@PEG not only acted as the contrast agents for T1-weighted MRI (relaxivity value of 1.05 mM−1 s−1), but also converted cellular H2O2 into highly toxic hydroxyl radicals (·OH) mediated chemodynamic therapy (CDT). Moreover, Furthermore, Mn-Ti3C2@PEG can efficiently suppressed tumor-growth by PTT, due to the high photothermal conversion capability and photothermal stability. As a proof-of-concept model, the as-designed Mn-Ti3C2@PEG nanoplatform shows simultaneous MRI and dual-modal treatment for effective suppression of tumor with minimized side effects both in vitro and in vivo, indicating the great potential for clinical cancer theranostics.

Tumor-Microenvironment-Responsive Cascade Reactions by a Cobalt-Single-Atom Nanozyme for Synergistic Nanocatalytic Chemotherapy.

Nanocatalytic therapy, involving the nanozyme-triggered production of reactive oxygen species (ROS) in the tumor microenvironment (TME), has demonstrated potential in tumor therapy, but nanozymes still face challenges of activity and specificity that compromise the therapeutic efficacy. Herein, we report a strategy based on a single-atom nanozyme to initiate cascade enzymatic reactions in the TME for tumor-specific treatment. The cobalt-single-atom nanozyme, with Co-N coordination on N-doped porous carbon (Co-SAs@NC), displays catalase-like activity that decomposes cellular endogenous H2 O2 to produce O2 , and subsequent oxidase-like activity that converts O2 into cytotoxic superoxide radicals to efficiently kill tumor cells. By incorporation with doxorubicin, the therapy achieves a significantly enhanced antitumor effect in vivo. Our findings show that cascade TME-specific catalytic therapy combined with chemotherapy is a promising strategy for efficient tumor therapy.

Tumor‐Microenvironment‐Responsive Cascade Reactions by a Cobalt‐Single‐Atom Nanozyme for Synergistic Nanocatalytic Chemotherapy

AbstractNanocatalytic therapy, involving the nanozyme‐triggered production of reactive oxygen species (ROS) in the tumor microenvironment (TME), has demonstrated potential in tumor therapy, but nanozymes still face challenges of activity and specificity that compromise the therapeutic efficacy. Herein, we report a strategy based on a single‐atom nanozyme to initiate cascade enzymatic reactions in the TME for tumor‐specific treatment. The cobalt‐single‐atom nanozyme, with Co−N coordination on N‐doped porous carbon (Co‐SAs@NC), displays catalase‐like activity that decomposes cellular endogenous H2O2 to produce O2, and subsequent oxidase‐like activity that converts O2 into cytotoxic superoxide radicals to efficiently kill tumor cells. By incorporation with doxorubicin, the therapy achieves a significantly enhanced antitumor effect in vivo. Our findings show that cascade TME‐specific catalytic therapy combined with chemotherapy is a promising strategy for efficient tumor therapy.

Hydrogen Peroxide Mediates Premature Senescence Caused by Darkness and Inorganic Nitrogen Starvation in Physcomitrium patens.

Leaf senescence accompanied by yellowing and Rubisco degradation occurs prematurely in response to various stresses. However, signaling pathways between stress perception and senescence responses are not understood fully, although previous studies suggest the involvement of reactive oxygen species (ROS). While investigating the physiological functions of autophagy in Physcomitrium patens using wild-type (WT) and autophagy-deficient atg5 strains, we found that Physcomitrium colonies senesce prematurely under dark or nitrogen-deficient conditions, with atg5 senescing earlier than WT. In the present study, we measured cellular H2O2, and examined whether H2O2 mediates premature senescence in Physcomitrium colonies. Methyl viologen, an ROS generator, increased cellular H2O2 levels and caused senescence-like symptoms. H2O2 levels were also elevated to the same plateau levels in WT and atg5 under dark or nitrogen-deficient conditions. The ROS scavenger N-acetylcysteine and the ROS source inhibitor carbonyl cyanide m-chlorophenylhydrazone inhibited the increase in H2O2 levels as well as senescence. Upon transfer to a nitrogen-deficient medium, H2O2 levels increased earlier in atg5 than in WT by ~18 h, whereas atg5 yellowed earlier by >2 days. We conclude that the increased H2O2 levels under dark or nitrogen-deficient conditions mediate premature senescence in Physcomitrium but do not explain the different senescence responses of WT and atg5 cells.

Dual stimulus-responsive core-satellite SERS nanoprobes for reactive oxygen species sensing during autophagy

As one kind of reactive oxygen species, hydrogen peroxide (H2O2) participated in various cellular biological processes including cell differentiation and inflammation responses. Abnormal H2O2 level is closely related to cancer and other diseases. Highly sensitive detection and monitoring H2O2 are of great importance for understanding the roles of H2O2 in cellular dynamic events. Herein, a novel dual stimulus-responsive core-satellite surface-enhanced Raman scattering (SERS) nanoprobe engineered with manganese dioxide (MnO2) and silver nanoparticles (Ag NPs) was constructed for sensitive H2O2 detection. The sensing strategy is based on the target-triggered degradation both of the “core” and “satellite”. In this system, the MnO2 core not only could be used as solid supporter to generate “hot spots” that can induce strong SERS signals, but also acted as the responsive unit for H2O2 sensing together with Ag NPs. A good linear relationship in the range from 1 to 100 μM and limit of detection of 7.44 μM were obtained. Moreover, the nanosensor possessed good repeatability. Based on this strategy, the sensitive detection of cellular H2O2 was achieved. Furthermore, the SERS-based H2O2 monitoring during the starvation-induced autophagy was realized by the developed nanoprobes. Our study provides a new way for sensitive H2O2 detection and opens a new avenue for sensing and detection of other biomolecules.

PDGFB targeting biodegradable FePt alloy assembly for MRI guided starvation-enhancing chemodynamic therapy of cancer

The application of chemodynamic therapy (CDT) for cancer is a serious challenge owing to the low efficiency of the Fenton catalyst and insufficient H2O2 expression in cells. Herein, we fabricated a PDGFB targeting, biodegradable FePt alloy assembly for magnetic resonance imaging (MRI)-guided chemotherapy and starving-enhanced chemodynamic therapy for cancer using PDGFB targeting, pH-sensitive liposome-coated FePt alloys, and GOx (pLFePt-GOx). We found that the Fenton-catalytic activity of FePt alloys was far stronger than that of traditional ultrasmall iron oxide nanoparticle (UION). Upon entry into cancer cells, pLFePt-GOx nanoliposomes degraded into many tiny FePt alloys and released GOx owing to the weakly acidic nature of the tumor microenvironment (TME). The released GOx-mediated glucose consumption not only caused a starvation status but also increased the level of cellular H2O2 and acidity, promoting Fenton reaction by FePt alloys and resulting in an increase in reactive oxygen species (ROS) accumulation in cells, which ultimately realized starving-enhanced chemodynamic process for killing tumor cells. The anticancer mechanism of pLFePt-GOx involved ROS-mediated apoptosis and ferroptosis, and glucose depletion-mediated starvation death. In the in vivo assay, the systemic delivery of pLFePt-GOx showed excellent antitumor activity with low biological toxicity and significantly enhanced T2-weighted magnetic resonance imaging (MRI) signal of the tumor, indicating that pLFePt-GOx can serve as a highly efficient theranostic tool for cancer. This work thus describes an effective, novel multi-modal cancer theranostic system.

Melatonin modulates Nrf2 activity to protect porcine pre-pubertal Sertoli cells from the abnormal H2 O2 generation and reductive stress effects of cadmium.

Melatonin (MLT) is a cytoprotective agent holding potential to prevent cadmium (Cd) toxicity and its impact in testicular function and fertility. In this study, we explored such potential in porcine pre‐pubertal Sertoli cells (SCs). Cd toxicity resulted in impaired SC viability and function, abnormal cellular H2O2 generation and efflux, and induction of reductive stress by the upregulation of Nrf2 expression and activity, cystine uptake and glutathione biosynthesis, glutathione‐S‐transferase P (GSTP) expression, and protein glutathionylation inhibition. Cd toxicity also stimulated the activity of cellular kinases (MAPK‐ERK1/2 and Akt) and NFkB transcription factor, and cJun expression was increased. MLT produced a potent cytoprotective effect when co‐administered with Cd to SCs; its efficacy and the molecular mechanism behind its cytoprotective function varied according to Cd concentrations. However, a significant restoration of cell viability and function, and of H2O2 levels, was observed both at 5 and 10 μM Cd. Mechanistically, these effects of MLT were associated with a significant reduction of the Cd‐induced activation of Nrf2 and GSTP expression at all Cd concentrations. CAT and MAPK‐ERK1/2 activity upregulation was associated with these effects at 5 μM Cd, whereas glutathione biosynthesis and efflux were involved at 10 μM Cd together with an increased expression of the cystine transporter xCT, of cJun and Akt and NFkB activity. MLT protects SCs from Cd toxicity reducing its H2O2 generation and reductive stress effects. A reduced activity of Nrf2 and the modulation of other molecular players of MLT signaling, provide a mechanistic rational for the cytoprotective effect of this molecule in SCs.

Fe[sbnd]N[sbnd]C single atom nanozymes with dual enzyme-mimicking activities for colorimetric detection of hydrogen peroxide and glutathione

H2O2 and glutathione (GSH) are critical redox molecules in the organism. Abnormal levels of cellular H2O2 and GSH are closely related to some diseases. Thus, it is imperative to detect H2O2 and GSH efficiently. In this work, FeNC single atom nanozymes (SANs) with both peroxidase and oxidase-mimicking activities were successfully prepared with the help of formamide condensation by one-step hydrothermal method. The FeNC SANs show excellent peroxidase-like activity, which possess a higher affinity for H2O2 and 3,3′,5,5′-tetramethylbenzidine (TMB) than horseradish peroxidase (HRP). Then, based on the chromogenic reaction of TMB, a colorimetric biosensor to detect H2O2 and GSH was developed. This biosensor has the linear ranges of 10–600 μmol/L for H2O2 with a low detection limit of 4.360 μmol/L and 100–400 μmol/L for GSH with a low detection limit of 78.33 μmol/L. Besides, this colorimetric biosensor exhibited a good recovery of H2O2 and GSH in diluted human serum. Finally, the FeNC SANs were encapsulated into agar gel to self-quantitatively detect GSH by naked eyes. This work provides a non-pyrolytic way to prepare SANs, which broadens the synthetic method of SANs and may promote the development of SANs for biosensor application.

Peroxisome-Derived Hydrogen Peroxide Modulates the Sulfenylation Profiles of Key Redox Signaling Proteins in Flp-In T-REx 293 Cells.

The involvement of peroxisomes in cellular hydrogen peroxide (H2O2) metabolism has been a central theme since their first biochemical characterization by Christian de Duve in 1965. While the role of H2O2 substantially changed from an exclusively toxic molecule to a signaling messenger, the regulatory role of peroxisomes in these signaling events is still largely underappreciated. This is mainly because the number of known protein targets of peroxisome-derived H2O2 is rather limited and testing of specific targets is predominantly based on knowledge previously gathered in related fields of research. To gain a broader and more systematic insight into the role of peroxisomes in redox signaling, new approaches are urgently needed. In this study, we have combined a previously developed Flp-In T-REx 293 cell system in which peroxisomal H2O2 production can be modulated with a yeast AP-1-like-based sulfenome mining strategy to inventory protein thiol targets of peroxisome-derived H2O2 in different subcellular compartments. By using this approach, we identified more than 400 targets of peroxisome-derived H2O2 in peroxisomes, the cytosol, and mitochondria. We also observed that the sulfenylation kinetics profiles of key targets belonging to different protein families (e.g., peroxiredoxins, annexins, and tubulins) can vary considerably. In addition, we obtained compelling but indirect evidence that peroxisome-derived H2O2 may oxidize at least some of its targets (e.g., transcription factors) through a redox relay mechanism. In conclusion, given that sulfenic acids function as key intermediates in H2O2 signaling, the findings presented in this study provide valuable insight into how peroxisomes may be integrated into the cellular H2O2 signaling network.

Ac/Ds-Induced Receptor-like Kinase Genes Deletion Provides Broad-Spectrum Resistance to Bacterial Blight in Rice.

Rice bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) seriously affects rice yield production. The discovery and application of broad-spectrum resistance genes are of great advance for disease resistance breeding. Previously, we identified that multiple receptor-like kinase (RLK) family gene deletions induced by the Ac/Ds system resulted in a lesion mimic symptom. In this study, the mutant #29 showed that this lesion mimic symptom was isolated. Further analysis identified that four RLK genes (RLK19-22) were deleted in the #29 mutant. The #29 mutant exhibited broad-spectrum resistance to Xoo and subsequent analyses identified that pathogenesis-related genes PR1a, PBZ1, and cellular H2O2 levels were significantly induced in the mutant compared to wild-type plants. A genetic analysis revealed that reconstruction of RLK20, RLK21, or RLK22 rescued the lesion mimic symptom of the #29 mutant, indicating that these three RLKs are responsible for broad-spectrum resistance in rice. Further yeast two hybrid and bimolecular fluorescence complementation assays demonstrated that RLK20 interacts with RBOHB, which is a ROS producer in plants. Compared to wild-type plants, the #29 mutant was more, while #29/RLK20 ox was less, susceptible to MV (methyl-viologen), an ROS inducer. Co-expression of RLK20 and RBOHB reduced RBOHB-promoted H2O2 accumulation in the cells. Taken together, our research indicated that the RLKs may inhibit RBOHB activity to negatively regulate rice resistance to Xoo. These results provide the theoretical basis and valuable information about the target genes necessary for the successful breeding of rice cultivars resistant to bacterial blight.

Brain Metabolite, Myo-inositol, Inhibits Catalase Activity: A Mechanism of the Distortion of the Antioxidant Defense System in Alzheimer's disease.

A strong correlation between brain metabolite accumulation and oxidative stress has been observed in Alzheimer’s disease (AD) patients. There are two central hypotheses for this correlation: (i) coaccumulation of toxic amyloid-β and Myo-inositol (MI), a significant brain metabolite, during presymptomatic stages of AD, and (ii) enhanced expression of MI transporter in brain cells during oxidative stress-induced volume changes in the brain. Identifying specific interactive effects of MI with cellular antioxidant enzymes would represent an essential step in understanding the oxidative stress-induced AD pathogenicity. This study demonstrated that MI inhibits catalase, an essential antioxidant enzyme primarily inefficient in AD, by decreasing its kcat (turnover number) and increasing Km (Michaelis–Menten constant) values. This inhibition of catalase by MI under in vivo studies increased cellular H2O2 levels, leading to decreased cell viability. Furthermore, MI induces distortion of the active heme center with an overall loss of structure and stability of catalase. MI also alters distances of the vital active site and substrate channel residues of catalase. The present study provides evidence for the involvement of MI in the inactivation of the antioxidant defense system during oxidative stress-induced pathogenesis of AD. Regulation of MI levels, during early presymptomatic stages of AD, might serve as a potential early-on therapeutic strategy for this disease.

Molecular Basis for the Interaction of Catalase with d-Penicillamine: Rationalization of Some of Its Deleterious Effects.

d-Penicillamine (d-Pen) is a sulfur compound used in the management of rheumatoid arthritis, Wilson's disease (WD), and alcohol dependence. Many side effects are associated with its use, particularly after long-term treatment. However, the molecular basis for such side effects is poorly understood. Based on the well-known oxidase activity of hemoproteins and the participation of catalase in cellular H2O2 redox signaling, we posit that d-Pen could inactivate catalase, thus disturbing H2O2 levels. Herein, we report on the molecular basis that could partly explain the side effects associated with this drug compound, and we demonstrate that it induces the formation of compound II, a temporarily inactive state of the enzyme, through two distinct mechanisms. Initially, d-Pen reacts with native catalase and/or iron metal ions, used to mimic non-heme iron overload observed in long-term treated WD patients, to generate thiyl radicals. These radicals partake in a futile redox cycle, thus producing superoxide radical anions O2•- and hydrogen peroxide H2O2. Then, either H2O2 unexpectedly reacts with reduced CAT-Fe(II) to produce compound II or both aforementioned reactive oxygen species intervene in compound II generation through compound I formation and then reduction. These findings support the evidence that d-Pen could perturb H2O2 redox homeostasis through transient but recurring catalase inactivation, which may in part rationalize some deleterious effects observed with this therapeutic agent, as discussed.

The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?

Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H2O2). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxisomes are selectively removed by the autophagy-lysosome pathway. This process, known as “pexophagy,” may serve a protective role in curbing peroxisome-derived oxidative stress. Peroxisomes also have the intrinsic ability to mediate and modulate H2O2-driven processes, including (selective) autophagy. However, the molecular mechanisms underlying these phenomena are multifaceted and have only recently begun to receive the attention they deserve. This review provides a comprehensive overview of what is known about the bidirectional relationship between peroxisomal H2O2 metabolism and (selective) autophagy. After introducing the general concepts of (selective) autophagy, we critically examine the emerging roles of H2O2 as one of the key modulators of the lysosome-dependent catabolic program. In addition, we explore possible relationships among peroxisome functioning, cellular H2O2 levels, and autophagic signaling in health and disease. Finally, we highlight the most important challenges that need to be tackled to understand how alterations in peroxisomal H2O2 metabolism contribute to autophagy-related disorders.

The central role of NADPH depletion in MnTE-2-PyP-induced prostate cancer cell growth inhibition

Radiotherapy is commonly used in prostate cancer treatment. MnTE-2-PyP is a superoxide dismutase (SOD) mimic that can protect normal tissues from radiation toxicities while simultaneously promoting radiation-induced damage to cancer tissues. Previous work from our laboratory demonstrated that MnTE-2-PyP increased cellular H2O2 levels and led to protein oxidation and DNA damage in prostate cancer cells, which partially contributes to prostate cancer growth arrest. However, the central mechanisms by which MnTE-2-PyP reduces prostate cancer growth remain unclear. In this study, we identified that MnTE-2-PyP depleted cellular reductant levels, especially NADPH, in prostate cancer cells. Correspondingly, we observed a significant decrease in activity of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD), which are major cellular NADPH producing enzymes in the pentose phosphate pathway. A decrease of GSH/GSSG ratios were confirmed in MnTE-2-PyP-treated prostate cancer cells, which may result from the decreased glutathione reductase (GR) activity due to NADPH depletion. We also identified that MnTE-2-PyP with radiation significantly increased lipid peroxidation in prostate cancer cells and upregulated sphingomyelin synthesis, which could further consume available NADPH. Thus, MnTE-2-PyP treatment causes lower NADPH levels, resulting in more oxidative stress and membrane damage of prostate cancer cells.

Hydrogen sulphide and nitric oxide mitigate the negative impacts of waterlogging stress on wheat (Triticum aestivum L.).

Nitric oxide (NO) and hydrogen sulphide (H2 S) are important gaseous signalling molecules that regulate key physiochemical mechanisms of plants under environmental stresses. A number of attempts have been made to improve waterlogging tolerance in plants, but with limited success. Having said that, NO and H2 S are vital signalling molecules, but their role in mitigating waterlogging effects on crop plants is not well established. We investigated the efficacy of exogenous NO and H2 S to alleviate waterlogging effects in two wheat cultivars (Galaxy-2013 and FSD-2008). Waterlogging produced a noticeable reduction in plant growth, yield, chlorophyll, soluble sugars and free amino acids. Besides, waterlogging induced severe oxidative damage seen as higher cellular TBARS and H2 O2 content. Antioxidant enzyme activity increased together with a notable rise in Fe2+ and Mn2+ content. Proline content was higher in waterlogged plants compared with non-waterlogged plants. In contrast, waterlogging caused a substantial decline in endogenous levels of essential nutrients (K+ , Ca2+ and Mg2+ ). Waterlogged conditions led to Fe2+ and Mn2+ toxicity due to rapid reduction of Fe3+ and Mn3+ in the soil. Exogenous NO and H2 S significantly protected plants from waterlogging effects by enhancing the oxidative defence and regulating nutritional status. Besides, the protective effects of exogenous NO were more prominent as compared with effects of H2 S. Further, we did not study the effect of H2 S and NO on photosynthetic attributes and expression of stress-related genes. Therefore, future studies should examine the effects of H2 S and NO on wheat physiology and gene expression under waterlogging.

Silica Nanoparticles as a Probable Anti-Oomycete Compound Against Downy Mildew, and Yield and Quality Enhancer in Grapevines: Field Evaluation, Molecular, Physiological, Ultrastructural, and Toxicity Investigations.

Downy mildew is the most destructive disease of grapevines in the regions of relatively warm and humid climate causing up to 50% yield losses. Application of silicon- (Si-) based products have been extensively studied against various oomycete, fungal, bacterial, and viral plant diseases, but studies on Si application in their nanosize are limited. In this study, the field application of silica nanoparticles (SiNPs) on Thompson Seedless grapevines (H4 strain) infected with downy mildew was evaluated. In addition, molecular, physiological, ultrastructural, and toxicity investigations were also conducted. The obtained results revealed that spraying of grapevines with SiNPs at 150 ppm significantly overexpressed the transcription factor jasmonate and ethylene-responsive factor 3 recording 8.7-fold, and the defense-related genes β-1,3-glucanase (11-fold), peroxidase (10.7-fold) pathogenesis-related-protein 1 (10.6-fold), and chitinase (6.5-fold). Moreover, a reduction up to 81.5% in the disease severity was achieved in response to this treatment. Shoot length and yield per grapevine were considerably enhanced recording up to 26.3 and 23.7% increase, respectively. The berries quality was also improved. Furthermore, this treatment led to an enhancement in the photosynthetic pigments, induction of phenolic and ascorbic acid contents, an increase in the activity of peroxidase and polyphenol oxidase enzymes, and a reduction in the cellular electrolyte leakage, lipid peroxidation, and H2O2 content. Scanning electron microscopy observations showed an increase up to 86.6% in the number of closed stomata and a reduction up to 55% in the average stomatal pore area in response to this treatment. Observations of the transmission electron microscopy showed ultrastructural alterations in the cells of a grapevine leaf due to the infection with downy mildew, including plasmolysis and disruption of the cellular components, abnormal chloroplasts, and thickening of the cell wall and cell membrane. These abnormal alterations were reduced in response to SiNPs spray. In contrast, this study also showed that this treatment had considerable cytotoxic and genotoxic effects at this direct dose/concentration. So, additional investigations to determine the SiNPs residue in the produced edible plant parts are urgently needed. In addition, the pre-harvest interval, toxicity index, and risk assessment should be evaluated before any recommendation for use.

Uptake, translocation, phytotoxicity, and hormetic effects of titanium dioxide nanoparticles (TiO2NPs) in Nigella arvensis L.

The extensive application of titanium dioxide nanoparticles (TiO2NPs) in agro-industrial practices leads to their high accumulation in the environment or agricultural soils. However, their threshold and ecotoxicological impacts on plants are still poorly understood. In this study, the hormetic effects of TiO2NPs at a concentration range of 0–2500 mg/L on the growth, and biochemical and physiological behaviors of Nigella arvensis in a hydroponic system were examined for three weeks. The translocation of TiO2NPs in plant tissues was characterized through scanning and transmission electron microscopy (SEM and TEM). The bioaccumulation of total titanium (Ti) was quantified by inductively coupled plasma atomic emission spectroscopy (ICP-AES). Briefly, the elongation of roots and shoots and the total biomass growth were significantly promoted at 100 mg/L TiO2NPs. As the results indicated, TiO2NPs had a hormesis effect on the proline content, i.e., a stimulating effect at the low concentrations of 50 and 100 mg/L and an inhibiting effect in the highest concentration of 2500 mg/L. A biphasic dose-response was observed against TiO2NPs in shoot soluble sugar and protein contents. The inhibitory effects were detected at ≥1000 mg/L TiO2NPs, where the synthesis of chlorophylls and carotenoid was reduced. At 1000 mg/ L, TiO2NPs significantly promoted the cellular H2O2 generation, and increased the activities of antioxidant enzymes such as superoxide dismutase (SOD), ascorbate peroxidase (APX), and catalase (CAT). Furthermore, it enhanced the total antioxidant content (TAC), total iridoid content (TIC), and 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity. Overall, the study revealed the physiological and biochemical alterations in a medicinal plant affected by TiO2NPs, which can help to use these NPs beneficially by eliminating their harmful effects.

Integrative small RNA and transcriptome analysis provides insight into key role of miR408 towards drought tolerance response in cowpea

Drought stress response studies and overexpression of vun-miR408 proved it to be essential for abiotic stress tolerance in cowpea. Small RNA and transcriptome sequencing of an elite high-yielding drought-tolerant Indian cowpea cultivar, Pusa Komal revealed a differential expression of 198 highly conserved, 21 legume-specific, 14 less-conserved, and 10 novel drought-responsive microRNAs (miRNAs) along with 3391 (up-regulated) and 3799 (down-regulated) genes, respectively, in the leaf and root libraries. Among the differentially expressed miRNAs, vun-miR408-3p, showed an up-regulation of 3.53-log2-fold change under drought stress. Furthermore, laccase 12 (LAC 12) was identified as the potential target of vun-miR408-3p using 5' RNA ligase-mediated rapid amplification of cDNA ends. The stable transgenic cowpea lines overexpressing artificial vun-miR408-3p (OX-amiR408) displayed enhanced drought and salinity tolerance as compared to the wild-type plants. An average increase of 30.17% in chlorophyll, 26.57% in proline, and 27.62% in relative water content along with lesser cellular H2O2 level was observed in the transgenic lines in comparison with the wild-type plants under drought stress. Additionally, the scanning electron microscopic study revealed a decrease in the stomatal aperture and an increase in the trichome density in the transgenic lines. The expression levels of laccase 3 and laccase 12, the potential targets of miR408, related to lipid catabolic processes showed a significant reduction in the wild-type plants under drought stress and the transgenic lines, indicating the regulation of lignin content as a plausibly essential trait related to the drought tolerance in cowpea. Taken together, this study primarily focused on identification of drought-responsive miRNAs and genes in cowpea, and functional validation of role of miR408 towards drought stress response in cowpea.

Stress and Recovery Responses of Microcystis aeruginosa Exposed to Extreme Light for Different Durations

Cyanobacterial growth is a significant problem in most parts of the world. Control measures are necessary to suppress cyanobacterial growth in natural water bodies. When the control measures were discontinued, cyanobacteria growth rebounded quickly. This study was conducted to provide insight into the stress and recovery responses of cyanobacteria. Microcystis aeruginosa was exposed to extreme light for 8 days, and the changes in response to the light exposure were observed. Post-exposure recovery performances were accessed by allowing Cyanobacteria to recover under optimum conditions for 8 days. Extreme light exposure causes stress on M. aeruginosa, but by adjusting the growth, pigmentation, chlorophyll fluorescence, and antioxidant levels, M. aeruginosa surpasses the stress. M. aeruginosa showed sudden changes in parameters on the eighth day of extreme light exposure. The post-stress recovery capacity of M. aeruginosa was positively correlated with the exposure duration. These findings suggest that exposure to light stress causes hardening of M. aeruginosa. The inter-parameter relationships differed between the stress and recovery phases. Besides, non-photochemical quenching was strongly correlated with cellular H2O2 content, which can indirectly explain the oxidative stress status of M. aeruginosa. This study highlights the research requirement on the post-stress recovery capacity of M. aeruginosa.