In vivo Multifunctional Magnetic Resonance Center, West Virginia University School of Medicine, Morgantown, West Virginia, USA.
Center for Inhalation Toxicology, West Virginia University School of Medicine, Morgantown, West Virginia, USA.
Exp Physiol. 2024 Sep;109(9):1420-1425. doi: 10.1113/EP092064. Epub 2024 Aug 1.
The long-term consequences of electronic cigarette (Ecig) use in humans are not yet known, but it is known that Ecig aerosols contain many toxic compounds of concern. We have recently shown that Ecig exposure impairs middle cerebral artery (MCA) endothelial function and that it takes 3 days for MCA reactivity to return to normal. However, the sources contributing to impairment of the endothelium were not investigated. We hypothesized that the increased levels of oxidative stress markers in the blood are correlated with impaired MCA reactivity. We used electron paramagnetic resonance (EPR) spectroscopy to examine plasma from 4-month-old male Sprague-Dawley rats that were exposed to either air (n = 5) or 1 h Ecig exposure, after which blood samples were collected at varying times after exposure (i.e., 1-4, 24, 48 and 72 h postexposure, n = 4 or 5 in each time group). The EPR analyses were performed using the redox-sensitive hydroxylamine spin probe 1-hydroxy-3-carboxymethyl-2,2,5,5-tetramethyl-pyrrolidine (CMH) to measure the level of reactive oxidant species in the plasma samples. We found that EPR signal intensity from the CM radical was significantly increased in plasma at 1-4, 24 and 48 h (P < 0.05, respectively) and returned to control (air) levels by 72 h. When evaluating the EPR results with MCA reactivity, we found a significant negative correlation (Pearson's P = 0.0027). These data indicate that impaired cerebrovascular reactivity resulting from vaping is associated with the oxidative stress level (measured by EPR from plasma) and indicate that a single 1 h vaping session can negatively influence vascular health for up to 3 days after vaping. HIGHLIGHTS: What is the central question of this study? Does the time course of oxidative stress triggered by electronic cigarette exposure follow the cerebral vascular dysfunction? What is the main finding and its importance? Electron paramagnetic resonance analysis shows that the oxidative stress induced after a single 1 h exposure to electronic cigarette aerosol takes ≤72 h to return to normal, which mirrors the time course for vascular dysfunction in the middle cerebral artery that we have reported previously.
电子烟（Ecig）在人类中的长期影响尚不清楚，但已知 Ecig 气溶胶中含有许多令人关注的有毒化合物。我们最近发现，电子烟暴露会损害大脑中动脉（MCA）的内皮功能，并且需要 3 天时间才能使 MCA 反应恢复正常。但是，没有研究导致内皮功能障碍的来源。我们假设血液中氧化应激标志物水平的升高与 MCA 反应性受损有关。我们使用电子顺磁共振（EPR）光谱法检查了暴露于空气（n = 5）或 1 小时电子烟暴露的 4 个月大雄性 Sprague-Dawley 大鼠的血浆，此后在暴露后的不同时间（即暴露后 1-4、24、48 和 72 小时，每个时间组 n = 4 或 5）采集血样。EPR 分析使用氧化还原敏感的羟胺自旋探针 1-羟基-3-羧甲基-2,2,5,5-四甲基吡咯烷（CMH）进行，以测量血浆样品中反应性氧化剂的水平。我们发现，CM 自由基的 EPR 信号强度在 1-4、24 和 48 小时（分别为 P < 0.05）的血浆中显着增加，并且在 72 小时恢复到对照（空气）水平。当用 MCA 反应性评估 EPR 结果时，我们发现存在显着的负相关（Pearson P = 0.0027）。这些数据表明，电子烟引起的脑血管反应性受损与氧化应激水平（通过血浆中的 EPR 测量）有关，并表明单次 1 小时电子烟使用可在电子烟使用后长达 3 天内对血管健康产生负面影响。要点：本研究的核心问题是什么？电子烟暴露引起的氧化应激时间过程是否与脑血管功能障碍相符？主要发现及其重要性是什么？电子顺磁共振分析表明，单次 1 小时电子烟气溶胶暴露后诱导的氧化应激需要≤72 小时才能恢复正常，与我们之前报道的大脑中动脉血管功能障碍的时间过程相吻合。
