Oxidative Stress in Respiratory Disorders

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 2865

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Department of Physiology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, SK-036 01 Martin, Slovakia
Interests: chronic respiratory diseases
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Special Issue Information

Dear Colleagues,

Oxidative stress is linked with various acute and chronic respiratory disorders. Abundant production of oxidants is responsible for the damage of a variety of biomolecules that subsequently triggers distinct pathological changes in the lung. Generation of reactive oxygen and nitrogen species plays an important role in inflammation, endothelial dysfunction, and fibrotic changes in the lung including lung damage due to hypoxia/hyperoxia, mechanical ventilation, etc. In addition to acute lung injury from various reasons including COVID-19, oxidative stress represents one of the fundamental factors in the pathogenesis of chronic respiratory disorders such as bronchial asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, or lung silicosis. Moreover, oxidative stress is of great importance in premature neonates in which the damage of immature lung tissue may cause bronchopulmonary dysplasia, pulmonary hypertension and other serious complications. Understanding the role of oxidative stress in respiratory diseases has led to the administration of various antioxidants, some of which have exerted very promising effects.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning the importance of oxidative stress in respiratory disorders and perspective treatments diminishing the oxidative lung damage. This research can include both in vitro and in vivo studies relating to any of the following topics: oxidative stress in acute lung injury; oxidative stress in chronic respiratory diseases (asthma, COPD, pulmonary fibrosis, lung silicosis etc.); oxidative stress in premature neonates; antioxidant treatment in respiratory diseases.

Prof. Dr. Daniela Mokra
Guest Editor

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Keywords

  • oxidative stress
  • lung
  • reactive oxygen species
  • reactive nitrogen species
  • acute lung injury
  • asthma
  • COPD
  • lung fibrosis
  • pulmonary silicosis
  • premature neonate

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Published Papers (2 papers)

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Research

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15 pages, 270 KB  
Article
Characterization of Systemic Oxidative Stress in Asthmatic Adults Compared to Healthy Controls and Its Association with the Oxidative Potential of Particulate Matter Collected Using Personal Samplers
by Miguel Santibáñez, Adriana Núñez-Robainas, Esther Barreiro, Andrea Expósito, Juan Agüero, Juan Luis García-Rivero, Beatriz Abascal, Carlos Antonio Amado, Juan José Ruiz-Cubillán, Carmen Fernández-Sobaler, María Teresa García-Unzueta, José Manuel Cifrián and Ignacio Fernandez-Olmo
Antioxidants 2025, 14(4), 385; https://doi.org/10.3390/antiox14040385 - 25 Mar 2025
Cited by 1 | Viewed by 1120
Abstract
Inflammatory cell activation in asthma may lead to reactive oxygen species (ROS) overproduction with an imbalance between oxidant levels and antioxidant capacity, called oxidative stress (OS). Since particulate matter (PM) airborne exposure may also contribute to ROS generation, it is unclear whether PM [...] Read more.
Inflammatory cell activation in asthma may lead to reactive oxygen species (ROS) overproduction with an imbalance between oxidant levels and antioxidant capacity, called oxidative stress (OS). Since particulate matter (PM) airborne exposure may also contribute to ROS generation, it is unclear whether PM contributes more to OS than inflammatory cell activation. In our ASTHMA-FENOP study, which included 44 asthma patients and 37 matched controls, we aimed to characterize OS using five serum markers: total ROS content, protein carbonyl content, oxidized low-density lipoprotein (OxLDL), 8-hydroxydeoxyguanosine, and glutathione. Volunteers wore personal samplers for 24 h, collecting fine and coarse PM fractions separately, and the oxidative potential (OP) was determined using two methods. We observed differences between asthmatic and non-asthmatic volunteers in some OS markers, such as OxLDL, with an adjusted mean difference of 50,059.8 ng/mL (p < 0.001). However, we did not find an association between higher PM-OP and increased systemic OS. This suggests that at our PM-OP exposure levels, OS generated by the inflammatory cells themselves is more relevant than that generated by airborne PM. This supports the idea that asthma is a heterogeneous disease at the molecular level, mediated by inflammatory cell activation, and that OS may have potential clinical implications. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Disorders)

Review

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31 pages, 2843 KB  
Review
Respiratory Ciliary Beat Frequency in COPD: Balancing Oxidative Stress and Pharmacological Treatment
by Marta Joskova, Vladimira Sadlonova, Daniela Mokra, Ivan Kocan, Martina Sutovska, Karin Kackova and Sona Franova
Antioxidants 2025, 14(11), 1340; https://doi.org/10.3390/antiox14111340 - 6 Nov 2025
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Abstract
In chronic obstructive pulmonary disease (COPD), dysregulated calcium homeostasis, oxidative stress, and mucus hypersecretion converge to suppress ciliary beat frequency (CBF), thereby compromising mucociliary clearance (MCC). These mechanisms are subject to pharmacological modulation. Long-acting muscarinic antagonists (LAMAs) exert direct cilia-stimulatory effects and may [...] Read more.
In chronic obstructive pulmonary disease (COPD), dysregulated calcium homeostasis, oxidative stress, and mucus hypersecretion converge to suppress ciliary beat frequency (CBF), thereby compromising mucociliary clearance (MCC). These mechanisms are subject to pharmacological modulation. Long-acting muscarinic antagonists (LAMAs) exert direct cilia-stimulatory effects and may counteract pathogen-induced mucin overproduction without impairing clearance. Long-acting β2-agonists (LABAs) enhance ciliary activity through the cAMP–PKA–dynein (cyclic adenosine monophosphate–protein kinase A–dynein) signalling pathway. Inhaled corticosteroids (ICSs), although largely neutral on CBF, provide indirect protection by suppressing IL-13–driven inflammation. Phosphodiesterase (PDE)-4 inhibitors sustain intracellular cAMP and promote ciliary motility, though their clinical use remains limited by adverse effects. Emerging evidence suggests that dual and triple therapies may provide additive or synergistic benefits for preserving mucociliary function. Clinically, ex vivo CBF interpretation may be influenced by ongoing pharmacotherapy and tissue sampling site. Nasal brush samples may predominantly reflect systemic rather than inhaled therapy. Moreover, differences in PDE isoform expression between nasal and bronchial epithelium further complicate direct extrapolation of results. Rigorous patient stratification by treatment regimen is therefore essential to reconcile inconsistencies reported across studies. Ultimately, preservation of MCC in COPD depends on a delicate balance between oxidative stress and pharmacological modulation of ciliary function. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Disorders)
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