Abstract
Metabolites are essential intermediate products in metabolism, and metabolism dysregulation indicates different types of diseases. Previous studies have shown that cigarette smoke dysregulated metabolites; however, limited information is available with electronic cigarette (e-cig) vaping. We hypothesized that e-cig vaping and cigarette smoking alters systemic metabolites, and we propose to understand the specific metabolic signature between e-cig users and cigarette smokers. Plasma from non-smoker controls, cigarette smokers, and e-cig users was collected, and metabolites were identified by UPLC-MS (ultra-performance liquid chromatography mass spectrometer). Nicotine degradation was activated by e-cig vaping and cigarette smoking with increased concentrations of cotinine, cotinine N-oxide, (S)-nicotine, and (R)-6-hydroxynicotine. Additionally, we found significantly decreased concentrations in metabolites associated with tricarboxylic acid (TCA) cycle pathways in e-cig users versus cigarette smokers, such as d-glucose, (2R,3S)-2,3-dimethylmalate, (R)-2-hydroxyglutarate, O-phosphoethanolamine, malathion, d-threo-isocitrate, malic acid, and 4-acetamidobutanoic acid. Cigarette smoking significant upregulated sphingolipid metabolites, such as d-sphingosine, ceramide, N-(octadecanoyl)-sphing-4-enine, N-(9Z-octadecenoyl)-sphing-4-enine, and N-[(13Z)-docosenoyl]-sphingosine, versus e-cig vaping. Overall, e-cig vaping dysregulated TCA cycle-related metabolites while cigarette smoking altered sphingolipid metabolites. Both e-cig and cigarette smoke increased nicotinic metabolites. Therefore, specific metabolic signatures altered by e-cig vaping and cigarette smoking could serve as potential systemic biomarkers for early pathogenesis of cardiopulmonary diseases.
Highlights
E-cigarette (e-cig) vaping has been increasing rapidly in the United States during recent decades since e-cig is considered a relatively safer alternative to help quit smoking [1]
Our results found e-cig vaping is more associated with bioenergy synthesis (TCA cycle) than cigarette smoking, while cigarette smoking leads to upregulated sphingolipid pathways
We further applied a multivariate analysis via the principal component analysis (PCA) model to determine the significance of metabolomics profiling in our cohorts (Figure 1C,D)
Summary
E-cigarette (e-cig) vaping has been increasing rapidly in the United States during recent decades since e-cig is considered a relatively safer alternative to help quit smoking [1]. We have shown circulating biomarkers are increased from e-cig users or cigarette smokers, predicting the risk of lung and heart diseases [13,14]. Previous studies reported that e-cig vaping and cigarette smoking inhibited bioenergy synthesis and induced mitochondrial dysfunction [15,16]. No study is available to show the bioenergy synthesis-related circulating metabolites in e-cig users and cigarette smokers compared to healthy controls. We determined the dysregulation of sphingolipid metabolites in plasma from cigarette smokers or e-cig users. Our results showed that metabolites related to nicotine degradation are dysregulated in the plasma from both e-cig users and cigarette smokers. TCA cycle-related metabolites showed alternation only in the plasma of e-cig users, while sphingolipid metabolites presented dysregulation only in cigarette smokers’ plasma
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