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Biochem Biophys Res Commun. 2016 Sep 2;477(4):620-625. doi: 10.1016/j.bbrc.2016.06.109. Epub 2016 Jun 23.

Electronic cigarette aerosols and copper nanoparticles induce mitochondrial stress and promote DNA fragmentation in lung fibroblasts.

Author information

1
Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
2
Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA. Electronic address: irfan_rahman@urmc.rochester.edu.

Abstract

Oxidants or nanoparticles have recently been identified as constituents of aerosols released from various styles of electronic cigarettes (E-cigs). Cells in the lung may be directly exposed to these constituents and harbor reactive properties capable of incurring acute cell injury. Our results show mitochondria are sensitive to both E-cig aerosols and aerosol containing copper nanoparticles when exposed to human lung fibroblasts (HFL-1) using an Air-Liquid Interface culture system, evident by elevated levels of mitochondrial ROS (mtROS). Increased mtROS after aerosol exposure is associated with reduced stability of OxPhos electron transport chain (ETC) complex IV subunit and nuclear DNA fragmentation. Increased levels of IL-8 and IL-6 in HFL-1 conditioned media were also observed. These findings reveal both mitochondrial, genotoxic, and inflammatory stresses are features of direct cell exposure to E-cig aerosols which are ensued by inflammatory duress, raising a concern on deleterious effect of vaping.

KEYWORDS:

Electronic cigarettes; Inflammation; Mitochondria; Nanoparticles; OxPhos; Reactive oxygen species

PMID:
27343559
PMCID:
PMC4967027
DOI:
10.1016/j.bbrc.2016.06.109
[Indexed for MEDLINE]
Free PMC Article

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