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

被引:113
作者
Lerner, Chad A. [1 ]
Rutagarama, Pierrot [1 ]
Ahmad, Tanveer [1 ]
Sundar, Isaac K. [1 ]
Elder, Alison [1 ]
Rahman, Irfan [1 ]
机构
[1] Univ Rochester, Med Ctr, Dept Environm Med, Box 850,601 Elmwood Ave, Rochester, NY 14642 USA
关键词
Electronic cigarettes; Mitochondria; Reactive oxygen species; OxPhos; Nanoparticles; Inflammation; VAPOR EXTRACT; SMOKE;
D O I
10.1016/j.bbrc.2016.06.109
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:620 / 625
页数:6
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