Chen TH, Hsu CC, Chang CP, Huang CC, Wang YJ, et al.
Environmental pollution (Barking, Essex : 1987). Date of publication 2025 Sep 1;volume 380():126521.
1. Environ Pollut. 2025 Sep 1;380:126521. doi: 10.1016/j.envpol.2025.126521. Epub
2025 May 27.
Hyperbaric oxygen therapy attenuates carbon monoxide-induced lung injury by
restoring mitochondrial dynamics and suppressing Pink1/Parkin-mediated
mitophagy.
Chen TH(1), Hsu CC(2), Chang CP(3), Huang CC(4), Wang YJ(5).
Author information:
(1)Department of Environmental and Occupational Health, College of Medicine,
National Cheng Kung University, Tainan, Taiwan; Department of Medical Research,
Chi Mei Medical Center, Tainan, Taiwan.
(2)Department of Emergency Medicine, Chi Mei Medical Center, Tainan, Taiwan;
School of Medicine, College of Medicine, National Sun Yat-sen University,
Kaohsiung, Taiwan.
(3)Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan.
Electronic address: jessica.cpchang@gmail.com.
(4)Department of Emergency Medicine, Chi Mei Medical Center, Tainan, Taiwan;
School of Medicine, College of Medicine, National Sun Yat-sen University,
Kaohsiung, Taiwan; Department of Emergency Medicine, Kaohsiung Medical
University, Kaohsiung, Taiwan. Electronic address: jasonhuang0803@gmail.com.
(5)Department of Environmental and Occupational Health, College of Medicine,
National Cheng Kung University, Tainan, Taiwan. Electronic address:
yjwang@mail.ncku.edu.tw.
Carbon monoxide (CO), a major air pollutant from vehicle emissions, industrial
combustion, and indoor fuel use, poses significant environmental and public
health risks. Although acute carbon monoxide poisoning (COP) is well-documented,
the underlying mechanisms driving long-term pulmonary complications following CO
exposure remain poorly understood. Hyperbaric oxygen therapy (HBOT) is the
standard treatment for COP, primarily for its ability to eliminate
carboxyhemoglobin and reduce oxidative stress. However, its role in preventing
long-term pulmonary dysfunction through the regulation of mitochondrial quality
control requires further investigation. This study aimed to elucidate how
mitochondrial dynamics and Pink1/Parkin-mediated mitophagy contribute to
CO-induced lung injury and to evaluate the therapeutic potential of HBOT.
Epidemiological analysis revealed an association between COP and an increased
chronic obstructive pulmonary disease (COPD) risk. In a rat model, CO exposure
led to emphysematous lung damage, persistent cytokine storms, and immune
dysregulation. CD86+ and CD163+ macrophages and neutrophils were found in both
bronchoalveolar lavage fluid and lung parenchyma, coexpressing pro-inflammatory
cytokines (e.g., CCL5, CCL20, IL-1β, IL-10, IL-17). Alveolar barrier integrity
was disrupted by downregulation of tight junction proteins ZO-1 and claudin 3.
In alveolar type II cells, mitochondrial dynamics were impaired (decreased Opa1,
increased Drp1), with concurrent activation of Pink1/Parkin-mediated mitophagy,
pyroptosis, and apoptosis. These alterations led to alveolar damage and
pulmonary dysfunction, including increased airway resistance, compliance, and
hyperinflation-hallmarks of COPD-like pathology. Notably, HBOT reversed these
changes by restoring mitochondrial homeostasis, suppressing cell death pathways,
reducing inflammation, and improving lung function. These findings provide novel
insights into the role of mitochondrial dynamics and selective mitophagy in the
pathogenesis of CO-induced lung injury. It also underscores the therapeutic
potential of HBOT in preventing and controlling long-term pulmonary
complications.
Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.
DOI: 10.1016/j.envpol.2025.126521
PMID: 40441279 [Indexed for MEDLINE]
Conflict of interest statement: Declaration of competing interest The authors
declare that they have no known competing financial interests or personal
relationships that could have appeared to influence the work reported in this
paper.
