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1. ASCORBATE PEROXIDASE6 delays the onset of age-dependent leaf senescence

   https://doi.org/10.1093/plphys/kiaa031  

   Chen, Changming; Galon, Yael; Rahmati Ishka, Maryam; Malihi, Shimrit; Shimanovsky, Vladislava; Twito, Shir; Rath, Abhishek; Vatamaniuk, Olena K; Miller, Gad (November 2020, Plant Physiology)

   null (Ed.)

   Abstract Age-dependent changes in reactive oxygen species (ROS) levels are critical in leaf senescence. While H2O2-reducing enzymes such as catalases and cytosolic ASCORBATE PEROXIDASE1 (APX1) tightly control the oxidative load during senescence, their regulation and function are not specific to senescence. Previously, we identified the role of ASCORBATE PEROXIDASE6 (APX6) during seed maturation in Arabidopsis (Arabidopsis thaliana). Here, we show that APX6 is a bona fide senescence-associated gene. APX6 expression is specifically induced in aging leaves and in response to senescence-promoting stimuli such as abscisic acid (ABA), extended darkness, and osmotic stress. apx6 mutants showed early developmental senescence and increased sensitivity to dark stress. Reduced APX activity, increased H2O2 level, and altered redox state of the ascorbate pool in mature pre-senescing green leaves of the apx6 mutants correlated with the early onset of senescence. Using transient expression assays in Nicotiana benthamiana leaves, we unraveled the age-dependent post-transcriptional regulation of APX6. We then identified the coding sequence of APX6 as a potential target of miR398, which is a key regulator of copper redistribution. Furthermore, we showed that mutants of SQUAMOSA PROMOTER BINDING PROTEIN-LIKE7 (SPL7), the master regulator of copper homeostasis and miR398 expression, have a higher APX6 level compared with the wild type, which further increased under copper deficiency. Our study suggests that APX6 is a modulator of ROS/redox homeostasis and signaling in aging leaves that plays an important role in developmental- and stress-induced senescence programs. 

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2. Arylsulfonothioates: Thiol-Activated Donors of Hydropersulfides which are Excreted to Maintain Cellular Redox Homeostasis or Retained to Counter Oxidative Stress

   https://doi.org/10.1021/jacs.4c17661  

   Khodade, Vinayak S; Liu, Qi; Zhang, Chengximeng; Keceli, Gizem; Paolocci, Nazareno; Toscano, John P (March 2025, Journal of the American Chemical Society)

   Despite their biological significance, the study of hydropersulfides (RSSH) is often limited due to their inherent instability. Here, we introduce arylsulfonothioates as thiol activated RSSH donors and provide insight into cellular reactive sulfur species homeostasis. These precursors persulfidate physiologically relevant thiols (RSH) to form the corresponding RSSH. Real-time monitoring of hydrogen sulfide (H2S) generation via membrane inlet mass spectrometry (MIMS) was employed to follow RSSH production, revealing that electron-donating aryl substituents marginally slow RSSH release rates, whereas electron-withdrawing substituents slightly accelerate release. Furthermore, arylsulfonothioates with strong electron-withdrawing substituents offer superior protection against doxorubicin (DOX)-induced cardiotoxicity. Experiments using H9c2 cardiomyocytes affirmed the cell-permeability of arylsulfonothioates and their ability to increase intracellular RSSH levels and protein persulfidation levels. Notably, we observe the excretion of RSSH into the extracellular medium. Further investigations revealed the involvement of the cystine/glutamate antiporter SLC7A11, as cotreatment with its inhibitor, sulfasalazine, significantly reduce extracellular RSSH release. H9c2 cells exhibit tolerance to arylsulfonothioate 1g with an electronwithdrawing 4-cyano group at 1 mM; however, inhibition of the cystine antiporter results in a minor decrease in cell viability. Under oxidative stress conditions induced by DOX or hydrogen peroxide (H2O2), cotreatment with 1g diminishes the excretion of RSSH and confers cytoprotection against DOX or H2O2-mediated toxicity. Our findings show adaptive cellular responses to RSSH levels, demonstrating excretion under elevated conditions to maintain redox homeostasis and intracellular retention as a protective response during oxidative stress. 

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3. Magnaporthe oryzae nucleoside diphosphate kinase is required for metabolic homeostasis and redox‐mediated host innate immunity suppression

   https://doi.org/10.1111/mmi.14580  

   Rocha, Raquel O.; Wilson, Richard A. (September 2020, Molecular Microbiology)

   Abstract The fungusMagnaporthe oryzaecauses blast, the most devastating disease of cultivated rice. After penetrating the leaf cuticle,M. oryzaegrows as a biotroph in intimate contact with living rice epidermal cells before necrotic lesions develop. Biotrophic growth requires maintaining metabolic homeostasis while suppressing plant defenses, but the metabolic connections and requirements involved are largely unknown. Here, we characterized theM. oryzaenucleoside diphosphate kinase‐encoding geneNDK1and discovered it was essential for facilitating biotrophic growth by suppressing the host oxidative burst—the first line of plant defense. NDK enzymes reversibly transfer phosphate groups from tri‐ to diphosphate nucleosides. Correspondingly, intracellular nucleotide pools were perturbed inM. oryzaestrains lackingNDK1through targeted gene deletion, compared to WT. This affected metabolic homeostasis: TCA, purine and pyrimidine intermediates, and oxidized NADP⁺, accumulated in Δndk1. cAMP and glutathione were depleted. ROS accumulated in Δndk1hyphae. Functional appressoria developed on rice leaf sheath surfaces, but Δndk1invasive hyphal growth was restricted and redox homeostasis was perturbed, resulting in unsuppressed host oxidative bursts that triggered immunity. We conclude Ndk1 modulates intracellular nucleotide pools to maintain redox balance via metabolic homeostasis, thus quenching the host oxidative burst and suppressing rice innate immunity during biotrophy. 

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4. Zebra finches (Taeniopygia castanotis) display varying degrees of stress resilience in response to constant light

   https://doi.org/10.1016/j.ygcen.2024.114644  

   Pham, Kevin; Lazenby, Madeline; Yamada, KayLene; Lattin, Christine R; Wada, Haruka (January 2025, General and Comparative Endocrinology)

   The ability for traits to recover after exposure to stress varies depending on the magnitude, duration, or type of stressor. One such stressor is circadian rhythm disruption stemming from exposure to light at night. Circadian rhythm disruption may lead to long-term physiological consequences; however, the capacity in which individuals recover and display stress resilience is not known. Here, we exposed zebra finches (Taeniopygia castanotis) to constant light (24L:0D) or a regular light/dark cycle (14L:10D) for 23 days, followed by a recovery period for 12 days. We measured body mass, corticosterone, and glucose levels at multiple timepoints, and relative protein expression of glucocorticoid receptors at euthanasia. Body mass significantly increased over time in light-exposed birds compared to controls, but a 12-day recovery period reversed this increase. Baseline levels of circulating glucose decreased in light-exposed birds compared to controls, but returned to pretreatment levels after the 12-day recovery period. In contrast, the glucose stress response did not show a similar recovery trend, suggesting longer recovery is needed or that this is a persistent effect in light-exposed birds. Surprisingly, we did not detect any differences in baseline corticosterone or reactivity of the hypothalamic-pituitiary-adrenal (HPA) axis between groups throughout the experiment. Moreover, we did not detect differences between relative protein expression of glucocorticoid receptors or a relationship with HPA axis reactivity. Yet, we found a positive relationship between glucocorticoid receptors and the glucose stress response, but only in the light group. Our results indicate that physiological and morphological traits differ in their ability to recover in response to constant light and warrants further investigation on the mechanisms driving stress resilience under a disrupted circadian rhythm. 

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5. Electrochemical Reactions at the Boundary Areas Between Cold Atmospheric Pressure Plasma, Air, and Water

   https://doi.org/10.3390/plasma7040049  

   Thomas, Jamiah; Volkov, Alexander G (December 2024, Plasma)

   A cold atmospheric-pressure He-plasma jet (CAPPJ) interacts with air and water, producing reactive oxygen and nitrogen species (RONS), including biologically active ions, radicals, and molecules such as NOx, H2O2, HNO3, HNO2, and O3. These compounds can activate interfacial redox processes in biological tissues. The CAPPJ can oxidize N2 to HNO3 and water to H2O2 at the interface between plasma and water. It can also induce the oxidation of water-soluble redox compounds in various organisms and in vitro. This includes salicylic acid, hydroquinone, and mixtures of antioxidants such as L (+)-ascorbic acid sodium salt with NADPH. It can react with redox indicators, such as ferroin, in a three-phase system consisting of air, CAPPJ, and water. Without reducing agents in the water, the CAPPJ will oxidize the water and decrease the pH of the solution. When antioxidants such as ascorbate, 1,4-hydroquinone, or NADPH are present in the aqueous phase, the CAPPJ oxidizes these substances first and then oxidizes water to H2O2. The multielectron mechanisms of the redox reactions in the plasma-air/water interfacial area are discussed and analyzed. 

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