Abstract
E-cigarettes are widely believed to be safer than conventional cigarettes and have been even suggested as aids for smoking cessation. However, while reasonable with some regards, this judgment is not yet supported by adequate biomedical research data. Since bronchial epithelial cells are the immediate target of inhaled toxicants, we hypothesized that exposure to e-cigarettes may affect the metabolome of human bronchial epithelial cells (HBEC) and that the changes are, at least in part, induced by oxidant-driven mechanisms. Therefore, we evaluated the effect of e-cigarette liquid (ECL) on the metabolome of HBEC and examined the potency of antioxidants to protect the cells. We assessed the changes of the intracellular metabolome upon treatment with ECL in comparison of the effect of cigarette smoke condensate (CSC) with mass spectrometry and principal component analysis on air-liquid interface model of normal HBEC. Thereafter, we evaluated the capability of the novel antioxidant tetrapeptide O-methyl-l-tyrosinyl-γ-l-glutamyl-l-cysteinylglycine (UPF1) to attenuate the effect of ECL. ECL caused a significant shift in the metabolome that gradually gained its maximum by the 5th hour and receded by the 7th hour. A second alteration followed at the 13th hour. Treatment with CSC caused a significant initial shift already by the 1st hour. ECL, but not CSC, significantly increased the concentrations of arginine, histidine, and xanthine. ECL, in parallel with CSC, increased the content of adenosine diphosphate and decreased that of three lipid species from the phosphatidylcholine family. UPF1 partially counteracted the ECL-induced deviations, UPF1’s maximum effect occurred at the 5th hour. The data support our hypothesis that ECL profoundly alters the metabolome of HBEC in a manner, which is comparable and partially overlapping with the effect of CSC. Hence, our results do not support the concept of harmlessness of e-cigarettes.
Highlights
Electronic cigarettes or e-cigarettes as the major representative of the electronic nicotine delivery systems are rapidly gaining popularity, because they are trivially expected to be a relatively harmless alternative for conventional smoking [1]
Principal component analysis (PCA) revealed that e-cigarette liquid (ECL) caused fluctuations that gradually gained their first maximum by the 5th h, which has receded by the 7th h (Fig 1A)
Fluctuations in the metabolome caused by cigarette smoke condensate (CSC) were in the scale and directions comparable with those caused by the ECL (Fig 1B)
Summary
Electronic cigarettes or e-cigarettes as the major representative of the electronic nicotine delivery systems are rapidly gaining popularity, because they are trivially expected to be a relatively harmless alternative for conventional smoking [1]. E-cigarettes have already been proposed as a promising tool for smoking cessation [4,5,6], but, on the other hand, they are deemed as an attractive gateway into tobacco consumption and renormalization of smoking among the youth [7, 8]. In short-term studies, e-cigarettes have been shown to harm lung function to a lesser extent than does conventional smoking at a similar level of nicotine bioavailability [11], they are not harmless. An increase has been demonstrated in peripheral airway resistance after using e-cigarette and proposed escalating oxidative stress as one of the deleterious effects of the use of e-cigarettes [12], analogously to that rising from the combustive cigarettes
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