Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture. (1st June 2016)

• Record Type: Journal Article
• Authors: Teasdale, Jack E.; Newby, Andrew C.; Timpson, Nicholas J.; Munafò, Marcus R.; White, Stephen J.
• Is Part Of: Drug and alcohol dependence. Volume 163(2016)
• Page Start: 256
• Page End: 260
• Publication Date: 2016-06-01
• Subjects: Cigarettes -- E-cigarettes -- Human coronary artery cells -- Stress response; Drug abuse -- Periodicals; Alcoholism -- Periodicals; 616.86
• DOI: 10.1016/j.drugalcdep.2016.04.020
• Languages: English
• ISSNs: 0376-8716

Abstract

Highlights: Human coronary artery endothelial cells show a biological response to cigarette smoke. This response was not seen following exposure to e-cigarette aerosol. Using e-cigarettes instead of cigarettes may reduce immediate cardiovascular harms. Abstract: Background: It is generally acknowledged that e-cigarettes are unlikely to be as harmful as conventional cigarettes, but there is little data that quantifies their relative harms. We investigated the biological response to e-cigarette aerosol exposure (versus conventional cigarette smoke exposure) at the cellular level, by exposing human coronary artery endothelial cells (HCAEC) to aqueous filtered extracts of e-cigarette aerosol or cigarette smoke and looking at gene expression changes consistent with a stress response. This included genes controlled by the oxidant-stress sensing transcription factor NFR2 (NFE2L2), and cytochrome P450 family members. Methods: Cigarette smoke extract (CSE) was created using mainstream smoke from a single cigarette drawn through 10 ml of endothelial cell growth media MV2. Electronic cigarette aerosol extract (eCAE) was created using the same apparatus, using a constant power output of 10.8 w (4.2 V) and 18 mg/ml nicotine solution. eCAE was generated using 5 cycles of 5 s heat with at least 10 s in between each puff to allow the coil to cool, air being drawn through the device at 70 ml/minute. Results: HCAEC responded to the noxious components in CSE, resulting in activation of NRF2 and upregulation of cytochrome p450. However, eCAE did not induce NRF2 nuclear localisation, upregulation of NRF2-activated genes, or the upregulation of cytochrome p450. Conclusions: The use of e-cigarettes as a substitute for conventional cigarettes is likely to reduce immediate tobacco-related harm, at least with respect to cardiovascular harms.