ArticleAntioxidants & redox signaling2013
Disulfide bond as a switch for copper-zinc superoxide dismutase activity in asthma.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring Potential Stress Granule-Related Biomarkers in Childhood Asthma Using Integrated Bioinformatics and Machine Learning.Journal of inflammation research · 2026Article
- Mitochondrial DNA copy number variation in asthma risk, severity, and exacerbations.The Journal of allergy and clinical immunology · 2025Article
- Hispidulin Alleviates Mast Cell-Mediated Allergic Airway Inflammation through FcεR1 and Nrf2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Erythrocytes of Little Ground Squirrels Undergo Reversible Oxidative Stress During Arousal From Hibernation.Frontiers in physiology · 2021Article
- Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology.International journal of molecular sciences · 2020Review
- Genome-wide expression profiling reveals increased stability and mitochondrial energy metabolism of the human liver cell line HepaRG-CAR.Cytotechnology · 2020Article
- Bioenergetic Differences in the Airway Epithelium of LeanAntioxidants & redox signaling · 2019Article
- Copper ion / HRedox biology · 2019Article
- Tanshinone IIA attenuates ovalbumin-induced airway inflammation and hyperresponsiveness in a murine model of asthma.Iranian journal of basic medical sciences · 2019Article
- Attenuation of utero-toxicity, metabolic dysfunction and inflammation by soy protein concentrate in rats exposed to fluoridated water: consequence of hyperlipidemia in parallel with hypohomocysteinemia.Environmental science and pollution research international · 2018Article
- Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling.Molecular aspects of medicine · 2018Review
- The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation.Nature communications · 2018Article
- ROLE OF THIOLS IN OXIDATIVE STRESS.Current opinion in toxicology · 2018Article
- New Insights in Oxidant Biology in Asthma.Annals of the American Thoracic Society · 2016Review
- Coenzyme Q in asthma.American journal of respiratory and critical care medicine · 2015Article
- Insights into the role of the unusual disulfide bond in copper-zinc superoxide dismutase.The Journal of biological chemistry · 2015Article
- Redox imaging of inflammation in asthma.American journal of respiratory and critical care medicine · 2014Article
- SOD1 oxidation and formation of soluble aggregates in yeast: relevance to sporadic ALS development.Redox biology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
aimLoss of superoxide dismutase (SOD) activity is a defining biochemical feature of asthma. However, mechanisms for the reduced activity are unknown. We hypothesized that loss of asthmatic SOD activity is due to greater susceptibility to oxidative inactivation.
resultActivity assays of blood samples from asthmatics and healthy controls revealed impaired dismutase activity of copper-zinc SOD (CuZnSOD) in asthma. CuZnSOD purified from erythrocytes or airway epithelial cells from asthmatic was highly susceptible to oxidative inactivation. Proteomic analyses identified that inactivation was related to oxidation of cysteine 146 (C146), which is usually disulfide bonded to C57. The susceptibility of cysteines pointed to an alteration in protein structure, which is likely related to the loss of disulfide bond. We speculated that a shift to greater intracellular reducing potential might account for the change. Strikingly, measures of reduced and oxidized glutathione confirmed greater reducing intracellular state in asthma, compared with controls. Similarly, greater free thiol in CuZnSOD was confirmed by ~2-fold greater N-ethylmaleimide binding to C146 in asthma as compared with controls. INNOVATION: Greater reducing potential under a chronic inflammatory state of asthma, thus, leads to susceptibility of CuZnSOD to oxidative inactivation due to cleavage of C57-C146 disulfide bond and exposure of usually unavailable cysteines.
conclusionVulnerability of CuZnSOD influenced by redox likely amplifies injury and inflammation during acute asthma attacks when reactive oxygen species are explosively generated. Overall, this study identifies a new paradigm for understanding the chemical basis of inflammation, in which redox regulation of thiol availability dictates protein susceptibility to environmental and endogenously generated reactive species.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.