E-cigarette-induced Changes in Cell Stress and Mitochondrial Function.
Supporting Files
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February 2025
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Available in CDC Stacks on January 26, 2026, 12:00 AM
File Language:
English
Details
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Alternative Title:Free Radical Biology & Medicine, 2025, v. 228: E-cigarette-induced Changes in Cell Stress and Mitochondrial Function.
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Journal Article:Free Radical Biology & Medicine
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Personal Author:
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Description:Inhaling aerosols from electronic nicotine delivery systems, such as e-cigarettes (e-cigs), may pose health risks beyond those caused by nicotine intake. Exposure to e-cig aerosols can lead to the release of exosomes and metabolites into the bloodstream, potentially affecting mitochondrial physiology across the body, leading to chronic inflammatory diseases. In this study we assessed the effects of e-cig use by young healthy human subjects on the circulating exosome profile and markers of cell stress, and also defined the effects of e-cig user plasma on mitochondrial function in endothelial cells (EA. Hy 926) and epithelial cells (A549) via adoptive transfer. E-cig users had altered plasma exosome profiles, with significantly increased levels of cell free mitochondrial DNA (mtDNA), protein carbonyls, and 4-HNE relative to non-users. Plasma from e-cig users decreased maximal mitochondrial respiration and spare capacity of cells, while also increasing metabolic stress, as evidenced by changes in mitochondrial phenotype from basal to stressed in both endothelial and epithelial cells, which was corroborated by electron microscopy demonstrating structural changes in mitochondria. Mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) levels significantly increased in e-cig plasma-subjected cells. Overall, we identified alterations in plasma exosome profiles and increased markers of mitochondrial stress in e-cig users and evidence that circulating factors within plasma from e-cig users drives metabolic stress in endothelial and epithelial cells. Our results imply that e-cig use adversely affects mitochondrial function, leading to stress and potentially chronic inflammation across the body.
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Content Notes:Author manuscript
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Source:Free Radical Biology & Medicine, 2025, v. 228
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DOI:
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ISSN:0891-5849 ; 1873-4596
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Pubmed ID:39756490
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Pubmed Central ID:PMC12834502
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Document Type:
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Funding:U01 IP000040/IP/NCIRD CDC HHSUnited States/ ; I01 BX004767/BX/BLRD VAUnited States/ ; U01 IP000965/IP/NCIRD CDC HHSUnited States/ ; T32 HL166127/HL/NHLBI NIH HHSUnited States/ ; IK6 BX005229/BX/BLRD VAUnited States/ ; R01 HL137052/HL/NHLBI NIH HHSUnited States/ ; R21 AG058174/AG/NIA NIH HHSUnited States/ ; I01 BX001963/BX/BLRD VAUnited States/ ; K24 HL155884/HL/NHLBI NIH HHSUnited States/
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Genre:
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Pages in Document:329-338 (20 pdf pages)
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Volume:228
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Main Document Checksum:urn:sha-512:d20376b3158013779f78e0840442ec658169efba2bc135d6b2ad5d1972eb84852ef4c09b69d8957b23af937595a243165b3bc88b7aa2e7b0785051aceea603af
Supporting Files
File Language:
English
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