scholarly journals Effects of Salicylic Acid on the Metabolism of Mitochondrial Reactive Oxygen Species in Plants

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 341 ◽  
Author(s):  
Péter Poór

Different abiotic and biotic stresses lead to the production and accumulation of reactive oxygen species (ROS) in various cell organelles such as in mitochondria, resulting in oxidative stress, inducing defense responses or programmed cell death (PCD) in plants. In response to oxidative stress, cells activate various cytoprotective responses, enhancing the antioxidant system, increasing the activity of alternative oxidase and degrading the oxidized proteins. Oxidative stress responses are orchestrated by several phytohormones such as salicylic acid (SA). The biomolecule SA is a key regulator in mitochondria-mediated defense signaling and PCD, but the mode of its action is not known in full detail. In this review, the current knowledge on the multifaceted role of SA in mitochondrial ROS metabolism is summarized to gain a better understanding of SA-regulated processes at the subcellular level in plant defense responses.

2019 ◽  
Vol 201 (22) ◽  
Author(s):  
Laura Barrientos-Moreno ◽  
María Antonia Molina-Henares ◽  
Marta Pastor-García ◽  
María Isabel Ramos-González ◽  
Manuel Espinosa-Urgel

ABSTRACT Iron is essential for most life forms. Under iron-limiting conditions, many bacteria produce and release siderophores—molecules with high affinity for iron—which are then transported into the cell in their iron-bound form, allowing incorporation of the metal into a wide range of cellular processes. However, free iron can also be a source of reactive oxygen species that cause DNA, protein, and lipid damage. Not surprisingly, iron capture is finely regulated and linked to oxidative-stress responses. Here, we provide evidence indicating that in the plant-beneficial bacterium Pseudomonas putida KT2440, the amino acid l-arginine is a metabolic connector between iron capture and oxidative stress. Mutants defective in arginine biosynthesis show reduced production and release of the siderophore pyoverdine and altered expression of certain pyoverdine-related genes, resulting in higher sensitivity to iron limitation. Although the amino acid is not part of the siderophore side chain, addition of exogenous l-arginine restores pyoverdine release in the mutants, and increased pyoverdine production is observed in the presence of polyamines (agmatine and spermidine), of which arginine is a precursor. Spermidine also has a protective role against hydrogen peroxide in P. putida, whereas defects in arginine and pyoverdine synthesis result in increased production of reactive oxygen species. IMPORTANCE The results of this study show a previously unidentified connection between arginine metabolism, siderophore turnover, and oxidative stress in Pseudomonas putida. Although the precise molecular mechanisms involved have yet to be characterized in full detail, our data are consistent with a model in which arginine biosynthesis and the derived pathway leading to polyamine production function as a homeostasis mechanism that helps maintain the balance between iron uptake and oxidative-stress response systems.


2005 ◽  
Vol 4 (8) ◽  
pp. 1396-1402 ◽  
Author(s):  
Miguel A. Rodríguez-Gabriel ◽  
Paul Russell

ABSTRACT Exposure to certain metal and metalloid species, such as arsenic, cadmium, chromium, and nickel, has been associated with an increased risk of cancer in humans. The biological effects of these metals are thought to result from induction of reactive oxygen species (ROS) and inhibition of DNA repair enzymes, although alterations in signal transduction pathways may also be involved in tumor development. To better understand metal toxicity and its connection to ROS, we have compared the effects of arsenite and hydrogen peroxide in wild-type and mutant strains of the fission yeast Schizosaccharomyces pombe. An atf1Δ pap1Δ strain, which is defective in two transcription factors that control stress responses, is extremely sensitive to hydrogen peroxide but not to arsenite. A strain that lacks the transcription factor Zip1 has the opposite relationship. Spc1 (Sty1) mitogen-activated protein kinase (MAPK), a homologue of mammalian p38 MAPK, and the upstream MAPK kinase (MAPKK) Wis1 are essential for survival of both arsenite and hydrogen peroxide. Inactivation of two MAPKK kinases, Win1 and Wis4, almost completely eliminates Spc1 activation by arsenite, yet these cells survive arsenite treatment. The two-component phosphorelay protein Mcs4, which acts upstream of Win1 and Wis4 and is required for Spc1 activation in response to oxidative stress, is not required for Spc1 activation in response to arsenite. We conclude that the toxic effects of arsenic are not strongly connected to oxidative stress and that although Spc1 is activated by arsenic exposure, the basal activity of Spc1 is largely sufficient for the survival of arsenic.


2011 ◽  
Vol 56 (No. 11) ◽  
pp. 537-546 ◽  
Author(s):  
M. Sevcikova ◽  
H. Modra ◽  
A. Slaninova ◽  
Z. Svobodova

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  


2021 ◽  
Vol 22 (19) ◽  
pp. 10799
Author(s):  
Kozo Nakai ◽  
Daisuke Tsuruta

Oxygen in the atmosphere is a crucial component for life-sustaining aerobic respiration in humans. Approximately 95% of oxygen is consumed as energy and ultimately becomes water; however, the remaining 5% produces metabolites called activated oxygen or reactive oxygen species (ROS), which are extremely reactive. Skin, the largest organ in the human body, is exposed to air pollutants, including diesel exhaust fumes, ultraviolet rays, food, xenobiotics, drugs, and cosmetics, which promote the production of ROS. ROS exacerbate skin aging and inflammation, but also function as regulators of homeostasis in the human body, including epidermal keratinocyte proliferation. Although ROS have been implicated in various skin diseases, the underlying mechanisms have not yet been elucidated. Current knowledge on ROS-related and oxidative stress-related skin diseases from basic research to clinical treatment strategies are discussed herein. This information may be applied to the future treatment of skin diseases through the individual targeting of the ROS generated in each case via their inhibition, capture, or regulation.


2012 ◽  
Vol 447 (3) ◽  
pp. 381-391 ◽  
Author(s):  
Brian J. Reon ◽  
Khoa H. Nguyen ◽  
Gargi Bhattacharyya ◽  
Anne Grove

Deinococcus radiodurans exhibits extreme resistance to DNA damage and is one of only few bacteria that encode two Dps (DNA protection during starvation) proteins. Dps-1 was shown previously to bind DNA with high affinity and to localize to the D. radiodurans nucleoid. A unique feature of Dps-2 is its predicted signal peptide. In the present paper, we report that Dps-2 assembly into a dodecamer requires the C-terminal extension and, whereas Dps-2 binds DNA with low affinity, it protects against degradation by reactive oxygen species. Consistent with a role for Dps-2 in oxidative stress responses, the Dps-2 promoter is up-regulated by oxidative stress, whereas the Dps-1 promoter is not. Although DAPI (4′,6-diamidino-2-phenylindole) staining of Escherichia coli nucleoids shows that Dps-1 can compact genomic DNA, such nucleoid condensation is absent from cells expressing Dps-2. A fusion of EGFP (enhanced green fluorescent protein) to the Dps-2 signal peptide results in green fluorescence at the perimeter of D. radiodurans cells. The differential response of the Dps-1 and Dps-2 promoters to oxidative stress, the distinct cellular localization of the proteins and the differential ability of Dps-1 and Dps-2 to attenuate hydroxyl radical production suggest distinct functional roles; whereas Dps-1 may function in DNA metabolism, Dps-2 may protect against exogenously derived reactive oxygen species.


2018 ◽  
Vol 200 (7) ◽  
Author(s):  
Alisa P. Lehman ◽  
Sharon R. Long

ABSTRACTReactive oxygen species such as peroxides play an important role in plant development, cell wall maturation, and defense responses. During nodulation with the host plantMedicago sativa,Sinorhizobium meliloticells are exposed to H2O2in infection threads and developing nodules (R. Santos, D. Hérouart, S. Sigaud, D. Touati, and A. Puppo, Mol Plant Microbe Interact 14:86–89, 2001,https://doi.org/10.1094/MPMI.2001.14.1.86).S. meliloticells likely also experience oxidative stress, from both internal and external sources, during life in the soil. Here, we present microarray transcription data forS. melilotiwild-type cells compared to a mutant deficient in the key oxidative regulatory protein OxyR, each in response to H2O2treatment. Several alternative sigma factor genes are upregulated in the response to H2O2; the stress sigma generpoE2shows OxyR-dependent induction by H2O2, whilerpoH1expression is induced by H2O2irrespective of theoxyRgenotype. The activity of the RpoE2 sigma factor in turn causes increased expression of two more sigma factor genes,rpoE5andrpoH2. Strains with deletions ofrpoH1showed improved survival in H2O2as well as increased levels ofoxyRand total catalase expression. These results imply that ΔrpoH1strains are primed to deal with oxidative stress. This work presents a global view ofS. melilotigene expression changes, and of regulation of those changes, in response to H2O2.IMPORTANCELike all aerobic organisms, the symbiotic nitrogen-fixing bacteriumSinorhizobium melilotiexperiences oxidative stress throughout its complex life cycle. This report describes the global transcriptional changes thatS. melilotimakes in response to H2O2and the roles of the OxyR transcriptional regulator and the RpoH1 sigma factor in regulating those changes. By understanding the complex regulatory response ofS. melilotito oxidative stress, we may further understand the role that reactive oxygen species play as both stressors and potential signals during symbiosis.


Genetics ◽  
2020 ◽  
Vol 217 (2) ◽  
Author(s):  
Ziming Zhong ◽  
Bruce A McDonald ◽  
Javier Palma-Guerrero

Abstract Reactive oxygen species are toxic byproducts of aerobic respiration that are also important in mediating a diversity of cellular functions. Reactive oxygen species form an important component of plant defenses to inhibit microbial pathogens during pathogen–plant interactions. Tolerance to oxidative stress is likely to make a significant contribution to the viability and pathogenicity of plant pathogens, but the complex network of oxidative stress responses hinders identification of the genes contributing to this trait. Here, we employed a forward genetic approach to investigate the genetic architecture of oxidative stress tolerance in the fungal wheat pathogen Zymoseptoria tritici. We used quantitative trait locus (QTL) mapping of growth and melanization under axenic conditions in two cross-populations to identify genomic regions associated with tolerance to oxidative stress. We found that QTLs associated with growth under oxidative stress as well as inherent growth can affect oxidative stress tolerance, and we identified two uncharacterized genes in a major QTL associated with this trait. Our data suggest that melanization does not affect tolerance to oxidative stress, which differs from what was found for animal pathogens. This study provides a whole-genome perspective on the genetic basis of oxidative stress tolerance in a plant pathogen.


2015 ◽  
Vol 59 (9) ◽  
pp. 5420-5426 ◽  
Author(s):  
Bédis Dridi ◽  
Andréanne Lupien ◽  
Michel G. Bergeron ◽  
Philippe Leprohon ◽  
Marc Ouellette

ABSTRACTOxidants were shown to contribute to the lethality of bactericidal antibiotics in different bacterial species, including the laboratory strainStreptococcus pneumoniaeR6. Resistance to penicillin amongS. pneumoniaeR6 mutants was further shown to protect against the induction of oxidants upon exposure to unrelated bactericidal compounds. In the work described here, we expanded on these results by studying the accumulation of reactive oxygen species in the context of antibiotic sensitivity and resistance by includingS. pneumoniaeclinical isolates. InS. pneumoniaeR6, penicillin, ciprofloxacin, and kanamycin but not the bacteriostatic linezolid, erythromycin, or tetracycline induced the accumulation of reactive oxygen species. For the three bactericidal compounds, resistance to a single molecule prevented the accumulation of oxidants upon exposure to unrelated bactericidal antibiotics, and this was accompanied by a reduced lethality. This phenomenon does not involve target site mutations but most likely implicates additional mutations occurring early during the selection of resistance to increase survival while more efficient resistance mechanisms are being selected or acquired. Bactericidal antibiotics also induced oxidants in sensitiveS. pneumoniaeclinical isolates. The importance of oxidants in the lethality of bactericidal antibiotics was less clear than forS. pneumoniaeR6, however, since ciprofloxacin induced oxidants even in ciprofloxacin-resistantS. pneumoniaeclinical isolates. Our results provide a clear example of the complex nature of the mode of action of antibiotics. The adaptive approach to oxidative stress ofS. pneumoniaeis peculiar, and a better understanding of the mechanism implicated in response to oxidative injury should also help clarify the role of oxidants induced by antibiotics.


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