Mitochondrial dysfunction induced by E-cigarettes
Document Type
Review
Publication Date
1-1-2026
Abstract
E-cigarette use has been linked to mitochondrial dysfunction through exposure to reactive oxygen species (ROS), toxic aldehydes, metals, and flavoring agents. These constituents can damage mitochondrial DNA, impair oxidative phosphorylation, and disrupt calcium homeostasis, resulting in oxidative stress, inflammation, and programmed cell death. Mitochondrial impairment contributes to many systemic disorders, including respiratory, cardiovascular, and metabolic conditions. Preclinical findings suggest altered mitochondrial morphology, reduced adenosine triphosphate (ATP) production, and increased ROS, all of which can contribute to mitochondrial dysfunction following e-cigarette exposure. Certain flavorings and metals intensify these effects. While early human data suggest systemic mitochondrial stress, most research remains in vitro or animal-based. This review identifies mitochondrial dysfunction as a key mechanism in e-cigarette toxicity and calls for longitudinal research to elucidate its long-term health consequences.
Publication Title
Toxicology
ISSN
0300483X
DOI
10.1016/j.tox.2025.154339
Recommended Citation
Sailis, Ardie Barry; Noh, Muhamad Alfakri Bin Mat; Leo, Bey Fen; Faruqu, Farid Nazer; Yee, Anne; and Sim, Maw Shin, "Mitochondrial dysfunction induced by E-cigarettes" (2026). Research Publications (2026 to 2030). 261.
https://knova.um.edu.my/research_publications_2026_2030/261
Volume
519