Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture
| Autor: | Nicholas J. Timpson, Jack E. Teasdale, Marcus R. Munafò, Stephen J. White, Andrew C. Newby |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Short Communication Electronic Nicotine Delivery Systems 030204 cardiovascular system & hematology Pharmacology Brain and Behaviour Toxicology medicine.disease_cause law.invention Nicotine 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation law Smoke medicine Humans Pharmacology (medical) Sidestream smoke Cells Cultured Aerosols Cigarettes biology business.industry Stress response Smoking Tobacco and Alcohol Endothelial Cells Human coronary artery cells Cytochrome P450 Tobacco Products Coronary Vessels NFE2L2 3. Good health Oxidative Stress E-cigarettes Psychiatry and Mental health 030104 developmental biology biology.protein business Electronic cigarette Oxidative stress medicine.drug |
| Zdroj: | Teasdale, J E, Newby, A C, Timpson, N J, Munafò, M R & White, S J 2016, ' Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture ', Drug and Alcohol Dependence, vol. 163, pp. 256-260 . https://doi.org/10.1016/j.drugalcdep.2016.04.020 Drug and Alcohol Dependence |
| ISSN: | 0376-8716 |
| DOI: | 10.1016/j.drugalcdep.2016.04.020 |
| Popis: | 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. 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. |
| Databáze: | OpenAIRE |
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