Glutathione, Stress Responses, and Redox Signaling in Lung Inflammation

2005 ◽  
Vol 7 (1-2) ◽  
pp. 42-59 ◽  
Author(s):  
Irfan Rahman ◽  
Saibal K. Biswas ◽  
Luis A. Jimenez ◽  
Martine Torres ◽  
H.J. Forman
Keyword(s):  
Stress Responses ◽  
Lung Inflammation ◽  
Redox Signaling

scholarly journals Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity, and Aging

2018 ◽  
Author(s):  
Collin Y. Ewald
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Enzymatic Activity ◽  
Stress Responses ◽  
Healthy Aging ◽  
Model Organism ◽  
Redox Signaling ◽  
Small Gtpases ◽  
Endoplasmic Reticulum Membrane ◽  
Nadph Oxidases

An accumulating body of evidence suggests that physiological reactive oxygen species (ROS) generated by NADPH oxidases act as a redox signal to re-establish homeostasis, a capacity that progressively declines during aging, but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox to generate ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: 1) enzymatic activity to catalyze cross-linking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, 2) high ROS bursts/levels to kill pathogens, and 3) Redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress- and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases and their relevance for human aging are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

scholarly journals S-Nitrosoglutathione Reductase-Modulated Redox Signaling Controls Sodic Alkaline Stress Responses in Solanum lycopersicum L.

2014 ◽  
Vol 56 (4) ◽  
pp. 790-802 ◽  
Author(s):  
Biao Gong ◽  
Dan Wen ◽  
Xiufeng Wang ◽  
Min Wei ◽  
Fengjuan Yang ◽  
...  
Keyword(s):  
Solanum Lycopersicum ◽  
Stress Responses ◽  
Redox Signaling ◽  
Alkaline Stress ◽  
Solanum Lycopersicum L

scholarly journals Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Antioxidants ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. 130 ◽  
Author(s):  
Collin Ewald
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Enzymatic Activity ◽  
Stress Responses ◽  
Healthy Aging ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox Signaling ◽  
Small Gtpases ◽  
Endoplasmic Reticulum Membrane ◽  
Nadph Oxidases

An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (e.g., RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox from generating ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: (1) enzymatic activity to catalyze crosslinking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, (2) high ROS bursts/levels to kill pathogens, and (3) redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases, and their relevance for human aging, are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

scholarly journals Peroxisomes as Redox-Signaling Nodes in Intracellular Communication and Stress Responses

2021 ◽  
Author(s):  
Luisa M Sandalio ◽  
Maria Angeles Peláez-Vico ◽  
Eliana Molina-Moya ◽  
Maria C Romero-Puertas
Keyword(s):  
Stress Responses ◽  
Redox Signaling ◽  
Intracellular Communication

scholarly journals Redox signaling through zinc activates the radiation response in Deinococcus bacteria

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Romaric Magerand ◽  
Pascal Rey ◽  
Laurence Blanchard ◽  
Arjan de Groot
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Stress Responses ◽  
Redox Homeostasis ◽  
Redox Signaling ◽  
Molecular Signaling ◽  
Signaling Mechanism ◽  
Zinc Excess ◽  
Metalloprotease Activity ◽  
And Oxidative Stress

AbstractDeinococcus bacteria are extremely resistant to radiation and other DNA damage- and oxidative stress-generating conditions. An efficient SOS-independent response mechanism inducing expression of several DNA repair genes is essential for this resistance, and is controlled by metalloprotease IrrE that cleaves and inactivates transcriptional repressor DdrO. Here, we identify the molecular signaling mechanism that triggers DdrO cleavage. We show that reactive oxygen species (ROS) stimulate the zinc-dependent metalloprotease activity of IrrE in Deinococcus. Sudden exposure of Deinococcus to zinc excess also rapidly induces DdrO cleavage, but is not accompanied by ROS production and DNA damage. Further, oxidative treatment leads to an increase of intracellular free zinc, indicating that IrrE activity is very likely stimulated directly by elevated levels of available zinc ions. We conclude that radiation and oxidative stress induce changes in redox homeostasis that result in IrrE activation by zinc in Deinococcus. We propose that a part of the zinc pool coordinated with cysteine thiolates is released due to their oxidation. Predicted regulation systems involving IrrE- and DdrO-like proteins are present in many bacteria, including pathogens, suggesting that such a redox signaling pathway including zinc as a second messenger is widespread and participates in various stress responses.

Apoplastic and Chloroplastic Redox Signaling Networks in Plant Stress Responses

2013 ◽  
Vol 18 (16) ◽  
pp. 2220-2239 ◽  
Author(s):  
Maija Sierla ◽  
Moona Rahikainen ◽  
Jarkko Salojärvi ◽  
Jaakko Kangasjärvi ◽  
Saijaliisa Kangasjärvi
Keyword(s):  
Stress Responses ◽  
Plant Stress ◽  
Redox Signaling ◽  
Signaling Networks ◽  
Plant Stress Responses

Acquiring control: The evolution of ROS-Induced oxidative stress and redox signaling pathways in plant stress responses

2019 ◽  
Vol 141 ◽  
pp. 353-369 ◽  
Author(s):  
Muhammad Ansar Farooq ◽  
Adnan Khan Niazi ◽  
Javaid Akhtar ◽  
Saifullah ◽  
Muhammad Farooq ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Plant Stress ◽  
Redox Signaling ◽  
Plant Stress Responses
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