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Related Experiment Video

Updated: Jun 4, 2025

Generation of Electronic Cigarette Aerosol by a Third-Generation Machine-Vaping Device: Application to Toxicological Studies
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E-cigarette-induced changes in cell stress and mitochondrial function.

Ramamurthy Chitteti1, Juan Pablo Zuniga-Hertz1, Jorge A Masso-Silva2

  • 1VA San Diego Healthcare System, San Diego, CA, USA; Department of Anesthesiology, School of Medicine, University of California San Diego, USA.

Free Radical Biology & Medicine
|January 5, 2025
PubMed
Summary
This summary is machine-generated.

Electronic cigarette (e-cig) use alters blood exosomes and mitochondrial function. E-cig aerosols harm cells, increasing stress and inflammation risk.

Keywords:
Electronic (e)-cigaretteEndothelial cellsEpithelial cellsMetabolic stressMitochondriaReactive oxygen speciesTobacco

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Area of Science:

  • Biomedical Science
  • Toxicology
  • Cell Biology

Background:

  • Electronic nicotine delivery systems (e-cigarettes or e-cigs) are increasingly popular.
  • Inhaling e-cig aerosols may cause health issues beyond nicotine addiction.
  • E-cig aerosol exposure can impact cellular processes and lead to chronic diseases.

Purpose of the Study:

  • To investigate the effects of e-cig use on circulating exosome profiles in young adults.
  • To assess markers of cell stress in e-cig users.
  • To determine how plasma from e-cig users affects mitochondrial function in human cells.

Main Methods:

  • Analysis of plasma exosome profiles and biomarkers (mtDNA, protein carbonyls, 4-HNE) in e-cig users and non-users.
  • In vitro study using endothelial (EA.hy926) and epithelial (A549) cells exposed to plasma from e-cig users.
  • Assessment of mitochondrial respiration, metabolic stress, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) levels.

Main Results:

  • E-cig users exhibited altered plasma exosome profiles with increased cell-free mitochondrial DNA (mtDNA), protein carbonyls, and 4-HNE.
  • Plasma from e-cig users reduced maximal mitochondrial respiration and spare capacity in exposed cells.
  • Increased metabolic stress, altered mitochondrial morphology, elevated MMP, and heightened ROS levels were observed in cells exposed to e-cig user plasma.

Conclusions:

  • E-cig use leads to significant alterations in plasma exosome profiles and increased markers of mitochondrial stress.
  • Circulating factors in e-cig user plasma drive metabolic stress in endothelial and epithelial cells.
  • E-cig use adversely affects mitochondrial function, potentially contributing to chronic inflammation.