Electronic cigarette aerosols induce oxidative stress-dependent cell death and NF-κB mediated acute lung inflammation in mice

Ma, Tiancong; Wang, Xiang; Li, Liqiao; Sun, Bingbing; Zhu, Yifang; Xia, Tian

doi:10.1007/s00204-020-02920-1

Cited by 31 publications

(14 citation statements)

References 39 publications

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“…In human pulmonary artery smooth muscle cells, the balance of NF-κB activation and downstream signaling events of inflammation are also regulated by ALDH2 [ 51 ]. E-cigarette aerosol-induced lung injury has also been linked to oxidative stress and the pro-inflammatory NF-κB pathways [ 52 ]. In the context of our present study, ALDH2*2 mice demonstrate a higher level of NF-κB phosphorylation after e-cigarette exposure compared to wild type ALDH2 mice.…”

Section: Discussionmentioning

confidence: 99%

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

Zeng

Xiao

et al. 2022

Redox Biology

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Section: Discussionmentioning

confidence: 99%

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

Zeng

Xiao

et al. 2022

Redox Biology

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“…In human pulmonary artery smooth muscle cells, the balance of NF-κB activation and downstream signaling events of inflammation are regulated by ALDH2 [48]. E-cigarette aerosol-induced lung injury has also been linked to oxidative stress and the pro-inflammatory NF-κB pathways [49]. In the context of our present study, ALDH2*2 mice demonstrated a higher level of NF-κB phosphorylation induced from e-cigarette exposure compared with that in wild type ALDH2 mice.…”

Section: Discussionmentioning

confidence: 99%

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

Zeng

Xiao

Chen

et al. 2021

Preprint

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AimsE-cigarette aerosol containing aldehydes, including acetaldehyde, are metabolized by the enzyme aldehyde dehydrogenase 2 (ALDH2). However, little is known how aldehyde exposure from e-cigarettes, when coupled with an inactivating ALDH2 genetic variant, ALDH2*2 (present in 8% of the world population), affects cardiovascular oxidative stress. The aim of this study was to determine how e-cigarette aerosol exposure, when coupled with genetics, impacts cardiovascular oxidative stress in wild type ALDH2 and ALDH2*2 knock-in mice.Methods and ResultsUsing selective ion flow mass spectrometry, we determined that e-cigarette aerosol contains acetaldehyde that are 10-fold higher than formaldehyde or acrolein. Next, using wild type ALDH2 and ALDH2*2 knock-in rodents, we identified organ-specific differences in ALDH2 with the heart having ~1.5-fold less ALDH2 enzyme activity relative to the liver and lung. In isolated cardiac myocytes, acetaldehyde exposure (30 seconds, 0.1-1 μM) caused a 4-fold greater peak in calcium levels for ALDH2*2 relative to ALDH2 cardiomyocytes. ALDH2*2 cardiomyocytes exposed to acetaldehyde also demonstrated a 2-fold increase in ROS production and 2.5-fold increase in 4HNE protein adducts relative to ALDH2 cardiomyocytes. For intact rodents, ALDH2*2 knock-in mice exposed to e-cigarette aerosol had an increased heart rate beginning 5 days after exposure compared to wild type ALDH2 mice (775±30 bpm versus 679±33 bpm, respectively, *p<0.01, n=7-8/group). E-cigarette aerosol exposure also exacerbated oxidative stress in ALDH2*2 heart homogenates, including a 1.3-fold higher protein carbonyl level, a 1.7-fold higher lipid peroxide level and 1.5-fold greater phosphorylation of NF-κB relative to wild type ALDH2 homogenates.ConclusionsThe increased oxidative stress from e-cigarette aerosol aldehydes triggers the proinflammatory NF-κB pathway. As ALDH2 expression and activity is lower in the heart relative to the lung, the heart could be more susceptible to increases in cardiovascular oxidative stress from e-cigarette aerosol; particularly for those carrying an ALDH2*2 genetic variant which limits acetaldehyde metabolism.Graphical AbstractE-cigarette aerosol exposure triggers increases in ROS that lead to increased protein carbonylation, MDA production, and elevates phosphorylated NF-kB. This exposure to e-cigarette aerosol leads to increases in cardiovascular oxidative stress. For the ALDH2*2 variant, there is limited ability to metabolize the reactive aldehydes from e-cigarette aerosol and with increased levels of oxidative stress at baseline relative to wild type ALDH2, e-cigarette aerosol increased oxidative stress, protein carbonylation, and phosphorylation of NF-kB relative to wild type ALDH2 rodents.

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“…On the other hand, negative effects of VOCs on the airways have also been reported. VOCs coming from electronic cigarettes, synthetic material, and household materials, induced lung oxidative stress, changes in the lung miRNA expression, neutrophilic infiltration, and airway hyperreactivity in the mice [87][88][89][90][91].…”

Section: Volatile Organic Compounds and Polycyclic Aromatic Hydrocarbonsmentioning

confidence: 99%

Air Pollution and the Airways: Lessons from a Century of Human Urbanization

et al. 2021

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Since the industrial revolution, air pollution has become a major problem causing several health problems involving the airways as well as the cardiovascular, reproductive, or neurological system. According to the WHO, about 3.6 million deaths every year are related to inhalation of polluted air, specifically due to pulmonary diseases. Polluted air first encounters the airways, which are a major human defense mechanism to reduce the risk of this aggressor. Air pollution consists of a mixture of potentially harmful compounds such as particulate matter, ozone, carbon monoxide, volatile organic compounds, and heavy metals, each having its own effects on the human body. In the last decades, a lot of research investigating the underlying risks and effects of air pollution and/or its specific compounds on the airways, has been performed, involving both in vivo and in vitro experiments. The goal of this review is to give an overview of the recent data on the effects of air pollution on healthy and diseased airways or models of airway disease, such as asthma or chronic obstructive pulmonary disease. Therefore, we focused on studies involving pollution and airway symptoms and/or damage both in mice and humans.

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Electronic cigarette aerosols induce oxidative stress-dependent cell death and NF-κB mediated acute lung inflammation in mice

Cited by 31 publications

References 39 publications

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme

Air Pollution and the Airways: Lessons from a Century of Human Urbanization

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