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Mitochondrial Dysfunction Induced by E-Cigarettes
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DOI：10.1016/j.tox.2025.154339.png)
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Abstract
En 中文
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.
Keywords:
DNA
deoxyribonucleic acid
mtDNA
mitochondrial DNA
E-cigarette
electronic cigarette
E-liquid
electronic liquid
ROS
reactive oxygen species
ATP
adenosine triphosphate
COPD
chronic obstructive pulmonary disease
ETC
electron transport chain
mPTP
mitochondrial permeability transition pore
IL
interleukin
TLR
toll-like receptor
NNK
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone
NNN
N′-Nitrosonornicotine
mitochondrial dysfunction
mitochondrial diseases
oxidative stress
electronic cigarette
electronic nicotine delivery systems
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