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Environmental stress induces mitochondrial retrograde signals that prompt protective responses in plants. The elusive mitochondrial signal has now been uncovered in a new study, which identifies formation of reactive oxygen species inside mitochondria as the key trigger of stress signals., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Detecting reactive oxygen species (ROS) that play a critical role as redox modulators and signalling molecules in biological systems currently requires invasive methods such as ROS -specific indicators for imaging and quantification. We developed a non-invasive, real-time, label-free imaging technique for assessing the level of ROS in live cells and thawed cryopreserved tissues that is compatible with in-vivo imaging. The technique is based on autofluorescence multispectral imaging (AFMI) carried out in an adapted fluorescence microscope with an expanded number of spectral channels spanning specific excitation (365 nm-495 nm) and emission (420 nm-700 nm) wavelength ranges. We established a strong quantitative correlation between the spectral information obtained from AFMI and the level of ROS obtained from CellROX staining. The results were obtained in several cell types (HeLa, PANC1 and mesenchymal stem cells) and in live kidney tissue. Additioanly,two spectral regimes were considered: with and without UV excitation (wavelengths > 400 nm); the latter being suitable for UV-sensitive systems such as the eye. Data were analyzed by linear regression combined with an optimization method of swarm intelligence. This allowed the calibration of AFMI signals to the level of ROS with excellent correlation (R = 0.84, p = 0.00) in the entire spectral range and very good correlation (R = 0.78, p = 0.00) in the limited, UV-free spectral range. We also developed a strong classifier which allowed us to distinguish moderate and high levels of ROS in these two regimes (AUC = 0.91 in the entire spectral range and AUC = 0.78 for UV-free imaging). These results indicate that ROS in cells and tissues can be imaged non-invasively, which opens the way to future clinical applications in conditions where reactive oxygen species are known to contribute to progressive disease such as in ophthalmology, diabetes, kidney disease, cancer and neurodegenerative diseases., Competing Interests: Declaration of competing interest Authors declare no conflict of interest., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Alfred Russell Wallace was a field naturalist with a strong interest in general physiology. In this vein, he wrote that oxygen (O2), produced by green plants, is "the food of protoplasm, without which it cannot continue to live". Here we summarize current models relating body size to respiration rates (in the context of the metabolic scaling theory) and show that oxygen-uptake activities, measured at 21 vol.% O2, correlate closely with growth patterns at the level of specific organs within the same plant. Thus, whole plant respiration can change ontogenetically, corresponding to alterations in the volume fractions of different tissues. Then, we describe the evolution of cyanobacterial photosynthesis during the Paleoarchean, which changed the world forever. By slowly converting what was once a reducing atmosphere to an oxidizing one, microbes capable of O2-producing photosynthesis modified the chemical nature and distribution of the element iron (Fe), slowly drove some of the most ancient prokaryotes to extinction, created the ozone (O3) layer that subsequently shielded the first terrestrial plants and animals from harmful UV radiation, but also made it possible for Earth's forest to burn, sometimes with catastrophic consequences. Yet another paradox is that the most abundant protein (i.e., the enzyme Rubisco, Ribulose-1,5-biphosphate carboxylase/oxygenase) has a greater affinity for oxygen than for carbon dioxide (CO2), even though its function is to bind with the latter rather than the former. We evaluate this second "oxygen paradox" within the context of photorespiratory carbon loss and crop yield reduction in C3 vs. C4 plants (rye vs. maize). Finally, we analyze the occurrence of reactive oxygen species (ROS) as destructive by-products of cellular metabolism, and discuss the three "O2-paradoxa" with reference to A. R. Wallace's speculations on "design in nature".

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. Though the pathogenesis of AF is complex and is not completely understood, many studies suggest that oxidative stress is a major mechanism in pathophysiology of AF. Through multiple mechanisms, reactive oxygen species (ROS) lead to the formation of an AF substrate that facilitates the development and maintenance of AF. In this review article, we provide an update on the different mechanisms by which oxidative stress promotes atrial remodeling. We then discuss several therapeutic strategies targeting oxidative stress for the prevention or treatment of AF. Considering the complex biology of ROS induced remodeling, and the evolution of ROS sources and compartmentalization during AF progression, there is a definite need for improvement in timing, targeting and reduction of off-target effects of therapeutic strategies targeting oxidative injury in AF. • For this special issue, we provide an update on the mechanisms by which oxidative stress promotes atrial fibrillation (AF). • We then discuss contemporary therapeutic strategies targeting oxidative stress for the prevention or treatment of AF. • Finally, we describe gaps in current knowledge and identify potential targets for novel therapeutic strategies in AF. [ABSTRACT FROM AUTHOR]

Botrytis cinerea, a necrotrophic fungus responsible for grey rot disease, causes substantial economic losses. However, recent studies have discovered distinct non-sporogenic and non-infective isolates of this species, such as the B459 field strain. Examination of these isolates is particularly intriguing in the context of the development of methodological applications that could be useful in the biocontrol of this phytopathogenic species. This investigation revealed that B459 exhibited a reduced growth rate yet displayed enhanced resilience to stressors like oxidative stress agents, SDS, ethanol, and PhITC. Notably, its ability to generate reactive oxygen species (ROS) and acidic compounds, crucial in plant–pathogen interactions, was impacted. Bio-targeted toxin identification assays and the metabolomic study of extracts obtained from fermentations at seven and fourteen days revealed that this strain does not biosynthesize botrydial and derivatives neither botcinin family toxins. Furthermore, its inability to infect tomato fruits, grape, and gerbera petals coincides with its lack of toxin production under culture conditions typically adapted for reference strain B05.10. [ABSTRACT FROM AUTHOR]

The objective of the current review is to summarize the current state of optical methods in redox biology. It consists of two parts, the first is dedicated to genetically encoded fluorescent indicators and the second to Raman spectroscopy. In the first part, we provide a detailed classification of the currently available redox biosensors based on their target analytes. We thoroughly discuss the main architecture types of these proteins, the underlying engineering strategies for their development, the biochemical properties of existing tools and their advantages and disadvantages from a practical point of view. Particular attention is paid to fluorescence lifetime imaging microscopy as a possible readout technique, since it is less prone to certain artifacts than traditional intensiometric measurements. In the second part, the characteristic Raman peaks of the most important redox intermediates are listed, and examples of how this knowledge can be implemented in biological studies are given. This part covers such fields as estimation of the redox states and concentrations of Fe–S clusters, cytochromes, other heme-containing proteins, oxidative derivatives of thiols, lipids, and nucleotides. Finally, we touch on the issue of multiparameter imaging, in which biosensors are combined with other visualization methods for simultaneous assessment of several cellular parameters. [Display omitted] • Detailed classification of genetically encoded fluorescent redox biosensors. • Redox biosensors and fluorescence lifetime imaging microscopy (FLIM). • Raman spectroscopy for redox biology. [ABSTRACT FROM AUTHOR]

D-amino acid oxidase (DAO) is a flavoenzyme that metabolizes D-amino acids by oxidative deamination, producing hydrogen peroxide (H2O2) as a by-product. The generation of intracellular H2O2 may alter the redox-homeostasis mechanism of cells and increase the oxidative stress levels in tissues, associated with the pathogenesis of age-related diseases and organ decline. This study investigates the effect of DAO knockdown using clustered regularly interspaced short palindromic repeats (CRISPR) through an in silico approach on its protein-protein interactions (PPIs) and their potential roles in the process of aging. The target sequence and guide RNA of DAO were designed using the CCTop database, PPI analysis using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, Reactome biological pathway, protein docking using GalaxyTongDock database, and structure analysis. The translated target sequence of DAO lies between amino acids 43 to 50. The 10 proteins that were predicted to interact with DAO are involved in peroxisome pathways such as acyl-coenzyme A oxidase 1 (ACOX1), alanine-glyoxylate and serine-pyruvate aminotransferase (AGXT), catalase (CAT), carnitine O-acetyltransferase (CRAT), glyceronephosphate O-acyltransferase (GNPAT), hydroxyacid oxidase 1 (HAO1), hydroxyacid oxidase 2 (HAO2), trans-L-3-hydroxyproline dehydratase (L3HYPDH), polyamine oxidase (PAOX), and pipecolic acid and sarcosine oxidase (PIPOX). In summary, DAO mutation would most likely reduce activity with its interacting proteins that generate H2O2. However, DAO mutation may result in peroxisomal disorders, and thus, alternative techniques should be considered for an in vivo approach. [ABSTRACT FROM AUTHOR]

Aging is associated with a decline in mitochondrial function which may contribute to age-related diseases such as neurodegeneration, cancer, and cardiovascular diseases. Recently, mitochondrial Complex II has emerged as an important player in the aging process. Mitochondrial Complex II converts succinate to fumarate and plays an essential role in both the tricarboxylic acid (TCA) cycle and the electron transport chain (ETC). The dysfunction of Complex II not only limits mitochondrial energy production; it may also promote oxidative stress, contributing, over time, to cellular damage, aging, and disease. Intriguingly, succinate, the substrate for Complex II which accumulates during mitochondrial dysfunction, has been shown to have widespread effects as a signaling molecule. Here, we review recent advances related to understanding the function of Complex II, succinate signaling, and their combined roles in aging and aging-related diseases. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is one of the most toxic compounds released into our environment and is harmful to human health, urging the need to remediate Cd-polluted soils. To this end, it is important to increase our insight into the molecular mechanisms underlying Cd stress responses in plants, ultimately leading to acclimation, and to develop novel strategies for economic validation of these soils. Albeit its non-redox-active nature, Cd causes a cellular oxidative challenge, which is a crucial determinant in the onset of diverse signalling cascades required for long-term acclimation and survival of Cd-exposed plants. Although it is well known that Cd affects reactive oxygen species (ROS) production and scavenging, the contribution of individual organelles to Cd-induced oxidative stress responses is less well studied. Here, we provide an overview of the current information on Cd-induced organellar responses with special attention to redox biology. We propose that an integration of organellar ROS signals with other signalling pathways is essential to finetune plant acclimation to Cd stress. [Display omitted] • Cadmium exposure rapidly induces an oxidative challenge in plants. • Cadmium increases reactive oxygen species levels in different compartments. • Redox signals are integrated with pathways mediating acclimation to cadmium stress. [ABSTRACT FROM AUTHOR]

Small proline-rich proteins (SPRRPs) are traditionally known for their function in keratinocyte homeostasis. Recent evidence demonstrates their involvement in additional diverse physiological processes ranging from p53 signaling and direct prevention of DNA damage to bactericidal activities. We highlight these novel, intriguing roles of SPRRPs and discuss them in the context of relevant pathological conditions. [ABSTRACT FROM AUTHOR]

Combined stress has been seen as a major threat to world agriculture production. Maize is one of the leading cereal crops of the world due to its wide spectrum of growth conditions and is moderately sensitive to salt stress. A saline soil environment is a major factor that hinders its growth and overall yield and causes an increase in the concentration of micronutrients like boron, leading to excess over the requirement of the plant. Boron toxicity combined with salinity has been reported to be a serious threat to the yield and quality of maize. The response signatures of the maize plants to the combined effect of salinity and boron stress have not been studied well. We carried out an integrative systems-level analysis of the publicly available transcriptomic data generated on tolerant maize (Lluteño maize from the Atacama Desert, Chile) landrace under combined salt and boron stress. We identified significant biological processes that are differentially regulated in combined salt and boron stress in the leaves and roots of maize, respectively. Protein-protein interaction network analysis identified important roles of aldehyde dehydrogenase (ALDH), galactinol synthase 2 (GOLS2) proteins of leaf and proteolipid membrane potential regulator (pmpm4), metallothionein lea protein group 3 (mlg3), and cold regulated 410 (COR410) proteins of root in salt tolerance and regulating boron toxicity in maize. Identification of transcription factors coupled with regulatory network analysis using machine learning approach identified a few heat shock factors (HSFs) and NAC (NAM (no apical meristem, Petunia), ATAF1–2 (Arabidopsis thaliana activating factor), and CUC2 (cup-shaped cotyledon, Arabidopsis)) family transcription factors (TFs) to play crucial roles in salt tolerance, maintaining reactive oxygen species (ROS) levels and minimizing oxidative damage to the cells. These findings will provide new ways to design targeted functional validation experiments for developing multistress-resistant maize crops. [ABSTRACT FROM AUTHOR]

Nanomaterials can be engineered with distinctive properties for their use in agriculture, environment, medicine, cosmetics and household commodities. Nonetheless, knowledge on the toxicity of engineered nanomaterials is actually limited, and their potential adverse effects should not be overlooked. In particular, it is important to understand the dynamics and mechanism of nanotoxicity. Toxicity of engineered nanomaterials arises mainly from their ability to produce reactive oxygen species, their ease of absorption and distribution into various tissues, and their kinetics of elimination from the human body. Therefore, toxicity mechanisms should be tested in model biological systems, with focus on properties such as size, shape, surface modification, composition, and aggregation. Here we review the fundamentals of nanotoxicity, methods to assess the toxicity of engineered nanomaterials, approaches to reduce toxicity during synthesis, and prospects of engineered nanomaterials in nanomedicine. [ABSTRACT FROM AUTHOR]

An epigenetic landscape encompasses a series of dynamic interconnected mechanisms working together to fashion a diverse set of phenotypes from a singular genotype. The epigenetic plasticity observed in disease and development is facilitated by enzymes that create and remove covalent modifications to DNA and histones. Several important discoveries within the past decade have revealed that epigenetic control mechanisms are subject to redox regulation and mitochondrial-to-nuclear retrograde signaling. This has led to our current understanding that the writers and erasers of the epigenome are influenced by several levels of redox and metabolic control including the bioavailability of oxygen, nutrients, and metabolite co-factors necessary for optimal enzyme activity. Thus, these enzymes perceive a cell's redox state, metabolic status, and environmental signals to influence chromatin structure and accessibility to the transcriptional apparatus. Not only are the activities of epigenetic enzymes affected by cellular redox conditions, but also, in feedback loop fashion, genes encoding antioxidant enzymes as well as prooxidant enzymes can be altered in their expression patterns by epigenetic silencing mechanisms. The altered expression of the anti- and prooxidant genes can then contribute to the onset or progression of disease. Epigenetic regulation of gene expression by the confluence of redox biology and gene-environment interactions is an active area of research and our understanding of these links continues to evolve. Given the emergent importance of crosstalk between redox biology and epigenetic regulatory mechanisms, it is timely that this issue should explore the current state of knowledge on this topic and how changes in metabolism and redox flux can result in tectonic shifts of the epigenetic landscape. [Display omitted] • Epigenetic alterations are involved in the etiology of many human diseases. • Oxygen is a powerful environmental morphogen directing chromatin structure and function. • Epigenetic writers and erasers are influenced by metabolic cofactors and cellular redox. • Aberrant redox signaling can instigate the altered epigenotype in disease. [ABSTRACT FROM AUTHOR]

HSV-λ infection of the cornea causes a severe immunoinflammatory and vision-impairing condition called herpetic stromal keratitis (SK). The virus replication in corneal epithelium followed by neutrophil- and CD41 T cell-mediated inflammation plays a dominant role in SK. Although previous studies demonstrate critical functions of type I IFNs (IFN-α/β) in HSV-1 infection, the role of recently discovered IFN-λ (type III IFN), specifically at the corneal mucosa, is poorly defined. Our study using a mouse model of SK pathogenesis shows that HSV-1 infection induces a robust IFN-λ response compared with type I IFN production at the corneal mucosal surface. However, the normal progression of SK indicates that the endogenous IFN responses are insufficient to suppress HSV-1-induced corneal pathology. Therefore, we examined the therapeutic efficacy of exogenous rIFN-λ during SK progression. Our results show that rIFN-λ therapy suppressed inflammatory cell infiltration in the cornea and significantly reduced the SK pathologic condition. Early rIFN-λ treatment significantly reduced neutrophil and macrophage infiltration, and IL-6, IL-1β, and CXCL-1 production in the cornea. Notably, the virucidal capacity of neutrophils and macrophages measured by reactive oxygen species generation was not affected. Similarly, ex vivo rIFN-λ treatment of HSV-1-stimulated bone marrow-derived neutrophils significantly promoted IFN-stimulated genes without affecting reactive oxygen species production. Collectively, our data demonstrate that exogenous topical rIFN-λ treatment during the development and progression of SK could represent a novel therapeutic approach to control HSV-1-induced inflammation and associated vision impairment. [ABSTRACT FROM AUTHOR]

Despite extensive research on molecular pathways controlling the process of regeneration in model organisms, little is known about the actual initiation signals necessary to induce regeneration. Recently, the activation of ERK signaling has been shown to be required to initiate regeneration in planarians. However, how ERK signaling is activated remains unknown. Reactive Oxygen Species (ROS) are well-known early signals necessary for regeneration in several models, including planarians. Still, the probable interplay between ROS and MAPK/ERK has not yet been described. Here, by interfering with major mediators (ROS, EGFR and MAPK/ERK), we were able to identify wound-induced ROS, and specifically H2O2, as upstream cues in the activation of regeneration. Our data demonstrate new relationships between regeneration-related ROS production and MAPK/ERK activation at the earliest regeneration stages, as well as the involvement of the EGFR-signaling pathway. Our results suggest that (1) ROS and/or H2O2 have the potential to rescue regeneration after MEK-inhibition, either by H2O2-treatment or light therapy, (2) ROS and/or H2O2 are required for the activation of MAPK/ERK signaling pathway, (3) the EGFR pathway can mediate ROS production and the activation of MAPK/ERK during planarian regeneration. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) is an important signalling molecule employed by plants to control many physiological aspects. This review summarizes that crosstalk between NO/H2O2/Ca2+ signalling pathways that drive pollen tube for sexual reproduction in flowering plants. NO is produced in seeds by both enzymatic and non-enzymatic sources that control many physiological aspects of seeds. The interplay of NO and Reactive oxygen species are likely important players in hormonal crosstalk controlling seed germination and dormancy. Mechanism of seed germination and dormancy is mainly regulated by plant hormones like Abscisic acid (ABA) and Gibberellic acid (GA). Based on mode of action of NO with reference to triggering the germination of crop seeds under abiotic stress condition it is infer that there is a linkage between NO and plant growth regulator production. NO cross -talk with reactive oxygen species (ROS) during abiotic stress condition, modulate the light and hormone depended developmental process in the early stage of plant development. NO action to enhancing abiotic stress tolerance by improving antioxidant enzymes and protection against oxidative damage in many crops are discussed in detail. [ABSTRACT FROM AUTHOR]

Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic‐specific knowledgebase DES‐RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology. [ABSTRACT FROM AUTHOR]

Abstract The balance between reactive oxygen species and reactive nitrogen species production by the host and stress response by fungi is a key axis of the host-pathogen interaction. This review will describe emerging themes in fungal pathogenesis underpinning this axis. [ABSTRACT FROM AUTHOR]