Teasdale Jack E, Newby Andrew C, Timpson Nicholas J, Munafò Marcus R, White Stephen J
School of Clinical Sciences, University of Bristol, Bristol, UK.
MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; School of Social and Community Medicine, University of Bristol, Bristol, UK.
Drug Alcohol Depend. 2016 Jun 1;163:256-60. doi: 10.1016/j.drugalcdep.2016.04.020. Epub 2016 Apr 22.
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.
Cigarette smoke extract (CSE) was created using mainstream smoke from a single cigarette drawn through 10ml of endothelial cell growth media MV2. Electronic cigarette aerosol extract (eCAE) was created using the same apparatus, using a constant power output of 10.8w (4.2V) and 18mg/ml nicotine solution. eCAE was generated using 5 cycles of 5s heat with at least 10s in between each puff to allow the coil to cool, air being drawn through the device at 70ml/minute.
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.
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.
人们普遍认为电子烟的危害可能不像传统香烟那么大，但几乎没有数据能量化它们的相对危害。我们通过将人冠状动脉内皮细胞（HCAEC）暴露于电子烟气溶胶或香烟烟雾的水性过滤提取物中，并观察与应激反应一致的基因表达变化，在细胞水平上研究了对电子烟气溶胶暴露（与传统香烟烟雾暴露相比）的生物学反应。这包括由氧化应激感应转录因子NFR2（NFE2L2）控制的基因以及细胞色素P450家族成员。
使用从一支香烟吸出的主流烟雾通过10ml内皮细胞生长培养基MV2来制备香烟烟雾提取物（CSE）。使用相同的装置制备电子烟气溶胶提取物（eCAE），使用10.8w（4.2V）的恒定功率输出和18mg/ml的尼古丁溶液。eCAE通过5个5秒加热周期产生，每次抽吸之间至少间隔10秒以使线圈冷却，空气以70ml/分钟的速度通过该装置抽吸。
HCAEC对CSE中的有害成分有反应，导致NRF2激活和细胞色素p450上调。然而，eCAE并未诱导NRF2核定位、NRF2激活基因的上调或细胞色素p450的上调。
使用电子烟替代传统香烟可能会减少直接的烟草相关危害，至少在心血管危害方面。
