暴露于电子香烟的大鼠血浆中氧化应激的电子顺磁共振时程研究。

IF 2.6 4区 医学 Q2 PHYSIOLOGY Experimental Physiology Pub Date : 2024-08-01 DOI:10.1113/EP092064
Murugesan Velayutham, Amber Mills, Valery V. Khramtsov, I. Mark Olfert
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引用次数: 0

摘要

目前尚不清楚使用电子烟(Ecig)对人体的长期影响,但已知电子烟气溶胶中含有许多令人担忧的有毒化合物。我们最近的研究表明,接触电子烟会损害大脑中动脉(MCA)内皮功能,MCA反应性需要3天才能恢复正常。然而,我们并未研究导致内皮功能受损的原因。我们假设血液中氧化应激标记物水平的升高与 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,然后在暴露后的不同时间收集了血液样本(即暴露后 1-4、24、48 和 72 小时,每个时间组 n = 4 或 5)。使用对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 EPR 分析,以测量血浆样本中活性氧化物的水平。我们发现,在 1-4、24 和 48 小时内,血浆中 CM- 自由基的 EPR 信号强度明显增加(P
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An electron paramagnetic resonance time-course study of oxidative stress in the plasma of electronic cigarette exposed rats

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 (< 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 = 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.

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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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