E-cigarette exposure impairs skeletal muscle mitochondrial function in male mice

Authors

• Pavel Mazirka, Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida, USA.
• Jaewon Choi, Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA.
• Samuel Alvarez, Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA.
• Pascual Jahuey, Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida, USA.
• Kerri A. O'Malley, Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida, USA.
• Scott T. Robinson, Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida, USA. MaineHealth Maine Medical Center, Portland, Maine, USA.

Document Type

Article

Publication Date

3-2026

Institution/Department

MaineHealth Medical Group Academic Pathway

Journal Title

Physiological reports

MeSH Headings

Animals; Male; Mice; Mice, Inbred C57BL; Mitochondria, Muscle (metabolism, drug effects); Receptors, Aryl Hydrocarbon (metabolism, genetics); Muscle, Skeletal (metabolism, drug effects); Electronic Nicotine Delivery Systems; Cytochrome P-450 CYP1A1 (metabolism, genetics); Cell Line; Basic Helix-Loop-Helix Proteins (metabolism, genetics); E-Cigarette Vapor (toxicity); Cell Survival (drug effects); Vaping (adverse effects)

Abstract

While conventional tobacco-cigarette smoking continues to decline, e-cigarette (E-cig) use is rising, yet its physiological consequences remain poorly characterized. Chronic activation of the aryl hydrocarbon receptor (AHR) by tobacco smoke impairs skeletal muscle mitochondrial function. Here, we evaluated whether E-cig vapor elicits AHR activation and mitochondrial dysfunction in skeletal muscle. C2C12 mouse myoblasts were exposed to 1% dimethyl sulfoxide (vehicle), 0.02% tobacco-smoke condensate (TSC), or vape condensate (VC) at 0.006%, 0.06%, and 0.3%. Cell viability, AHR-pathway gene expression (Ahr, Ahrr, Cyp1a1), and mitochondrial respiration were assessed. Male C57BL/6J mice (12-16 weeks; n = 4-5/group) underwent acute 2-h or 4-week exposure to room air, tobacco smoke, or E-cig vapor. Serum cotinine, gastrocnemius AHR-pathway genes, muscle contractility, and mitochondrial function were evaluated. In myoblasts, 0.02% TSC and 0.3% VC upregulated Ahrr and Cyp1a1 (p <  0.0001) and reduced complex I state-3 respiration (p <  0.05) without affecting viability. In mice, acute exposure to tobacco smoke and E-cig vapor significantly increased serum cotinine (p <  0.0001), but only tobacco-smoke activated AHR-pathway. Chronic exposure to tobacco smoke and E-cig vapor reduced mitochondrial complex I and II state-3 respiration (p <  0.05), without altering muscle contractile function. These findings suggest that AHR-independent mechanisms contribute to mitochondrial dysfunction with E-cig vapor exposure.

First Page

e70797

Recommended Citation

Mazirka, Pavel; Choi, Jaewon; Alvarez, Samuel; Jahuey, Pascual; O'Malley, Kerri A.; and Robinson, Scott T., "E-cigarette exposure impairs skeletal muscle mitochondrial function in male mice" (2026). MaineHealth Maine Medical Center. 4718.
https://knowledgeconnection.mainehealth.org/mmc/4718