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Updated: Jun 5, 2025

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
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Oxidative Injury to Lung Mitochondrial DNA is a Key Contributor for the Development of Chemical Lung Injury

Shubham Dubey, Zhihong Yu, Emily Morgan Stephens

    Biorxiv : the Preprint Server for Biology
    |December 9, 2024
    PubMed

    Insights

    Inhaling chlorine gas damages mitochondrial DNA, causing lung injury and death. Restoring mitochondrial DNA repair enzyme OGG1 protected mice from lung damage and improved survival.

    Area of Science:

    • Toxicology
    • Mitochondrial Biology
    • Pulmonology

    Background:

    • Oxidant gases can cause lung injury, but their effect on mitochondrial DNA is unknown.
    • Mitochondrial DNA (mtDNA) damage is implicated in various diseases.

    Purpose of the Study:

    • To investigate the role of oxidant gas-induced mitochondrial genome damage in acute and chronic lung injury.
    • To explore the therapeutic potential of targeting mitochondrial DNA repair.

    Main Methods:

    • Mice were exposed to chlorine (Cl2) gas.
    • Mitochondrial DNA integrity, protein expression, and inflammatory markers were analyzed.
    • Mice received intranasal instillation of a mitochondrial-targeted OGG1 protein (mitoOGG1).

    Main Results:

    • Chlorine gas exposure led to loss of DNA glycosylase OGG1, mtDNA damage, and increased mortality.
    • Proteomics revealed alterations in lung mitochondrial proteins post-exposure.
    • mitoOGG1 treatment reduced mtDNA oxidative injury, lung inflammation, and injury severity, improving survival.

    Conclusions:

    • Mitochondrial genome injury is a critical factor in acute and chronic lung injury.
    • Targeting mitochondrial DNA repair pathways, such as with mitoOGG1, offers a potential therapeutic strategy for lung injury.

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