Abstract
BackgroundCigarette smoking is believed to cause oxidative stress by several mechanisms, including direct damage by radical species and the inflammatory response induced by smoking, and would therefore be expected to cause increased lipid peroxidation. The aim was to carry out the first study of the relationship of smoking in humans to the level of n-3 lipid peroxidation indexed by the level of ethane in exhaled breath.MethodsSamples of alveolar air were obtained from 11 smokers and 18 non-smokers. The air samples were analyzed for ethane using mass spectrometry.ResultsThe two groups of subjects were matched with respect to age and gender. The mean cumulative smoking status of the smokers was 11.8 (standard error 2.5) pack-years. The mean level of ethane in the alveolar breath of the group of smokers (2.53 (0.55) ppb) was not significantly different from that of the group of non-smokers (2.59 (0.29) ppb; p = 0.92). With all 29 subjects included, the Spearman rank correlation coefficient between ethane levels and cumulative smoking status was -0.11 (p = 0.58), while an analysis including only the smokers yielded a corresponding correlation coefficient of 0.11 (p = 0.75).ConclusionOur results show no evidence that cigarette smoking is related to increased n-3 lipid peroxidation as measured by expired ethane.
Highlights
Cigarette smoking is believed to cause oxidative stress by several mechanisms, including direct damage by radical species and the inflammatory response induced by smoking, and would be expected to cause increased lipid peroxidation
The smoking of cigarettes by humans is believed to cause oxidative stress by several mechanisms, including direct damage by radical species and the inflammatory response induced by smoking [1,2]: peroxyl radicals and reactive nitrogen species cause direct damage, stimulating lipid peroxidation, oxidizing and nitrating proteins, lipids and DNA bases; aldehydes can deplete GSH and modify protein -SH and -NH2 groups; cigarette smoke tar phase hydroquinone/quinine complexes diffuse across cell membranes and give rise to semiquinones, superoxide radicals (O2·-) and hydrogen peroxide
We report the first study of the relationship of smoking in humans to the level of n-3 lipid peroxidation indexed by the level of ethane in exhaled breath
Summary
Cigarette smoking is believed to cause oxidative stress by several mechanisms, including direct damage by radical species and the inflammatory response induced by smoking, and would be expected to cause increased lipid peroxidation. The aim was to carry out the first study of the relationship of smoking in humans to the level of n-3 lipid peroxidation indexed by the level of ethane in exhaled breath. Cigarette smoking would be expected to be associated with increased lipid peroxidation. It is possible to measure lipid peroxidation in humans using a non-invasive sensitive measure of free radical damage by analyzing directly the early products of oxidation in exhalant volatile hydrocarbons [3]. The automated thermal desorption tubes were desorbed onto the cold trap at 320°C, with the cold trap temperature being held at 5°C. Ethane (C2H6) was eluted at 2.6 min and identified and quantified by mass spectrometry at an m/z value of 30 by comparison with a standard curve (0–60 pmol) constructed from a C1–C6 alkane standard mix (Supelco, UK)
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