A comparison of oxidative stress in smokers and non-smokers: an in vivo human quantitative study of n-3 lipid peroxidation

<p>Abstract</p> <p>Background</p> <p>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 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 <it>n</it>-3 lipid peroxidation indexed by the level of ethane in exhaled breath.</p> <p>Methods</p> <p>Samples of alveolar air were obtained from 11 smokers and 18 non-smokers. The air samples were analyzed for ethane using mass spectrometry.</p> <p>Results</p> <p>The 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; <it>p </it>= 0.92). With all 29 subjects included, the Spearman rank correlation coefficient between ethane levels and cumulative smoking status was -0.11 (<it>p </it>= 0.58), while an analysis including only the smokers yielded a corresponding correlation coefficient of 0.11 (<it>p </it>= 0.75).</p> <p>Conclusion</p> <p>Our results show no evidence that cigarette smoking is related to increased <it>n</it>-3 lipid peroxidation as measured by expired ethane.</p

Evidence from in vivo 31-phosphorus magnetic resonance spectroscopy phosphodiesters that exhaled ethane is a biomarker of cerebral n-3 polyunsaturated fatty acid peroxidation in humans

<p>Abstract</p> <p>Background</p> <p>This study tested the hypothesis that exhaled ethane is a biomarker of cerebral <it>n</it>-3 polyunsaturated fatty acid peroxidation in humans. Ethane is released specifically following peroxidation of <it>n</it>-3 polyunsaturated fatty acids. We reasoned that the cerebral source of ethane would be the docosahexaenoic acid component of membrane phospholipids. Breakdown of the latter also releases phosphorylated polar head groups, giving rise to glycerophosphorylcholine and glycerophosphorylethanolamine, which can be measured from the 31-phosphorus neurospectroscopy phosphodiester peak. Schizophrenia patients were chosen because of evidence of increased free radical-mediated damage and cerebral lipid peroxidation in this disorder.</p> <p>Methods</p> <p>Samples of alveolar air were obtained from eight patients and ethane was analyzed and quantified by gas chromatography and mass spectrometry (<it>m</it>/<it>z </it>= 30). Cerebral 31-phosphorus spectra were obtained from the same patients at a magnetic field strength of 1.5 T using an image-selected <it>in vivo </it>spectroscopy sequence (TR = 10 s; 64 signal averages localized on a 70 × 70 × 70 mm³voxel). The quantification of the 31-phosphorus signals using prior knowledge was carried out in the temporal domain after truncating the first 1.92 ms of the signal to remove the broad component present in the 31-phosphorus spectra.</p> <p>Results</p> <p>The ethane and phosphodiester levels, expressed as a percentage of the total 31-phosphorus signal, were positively and significantly correlated (<it>r</it>_{<it>s </it>}= 0.714, <it>p </it>< 0.05).</p> <p>Conclusion</p> <p>Our results support the hypothesis that the measurement of exhaled ethane levels indexes cerebral <it>n</it>-3 lipid peroxidation. From a practical viewpoint, if human cerebral <it>n</it>-3 polyunsaturated fatty acid catabolism can be measured by ethane in expired breath, this would be more convenient than determining the area of the 31-phosphorus neurospectroscopy phosphodiester peak.</p

Cerebral spectroscopic and oxidative stress studies in patients with schizophrenia who have dangerously violently offended

<p>Abstract</p> <p>Background</p> <p>The aim of this study was to bring together all the results of <it>in vivo </it>studies of ethane excretion and cerebral spectroscopy in patients with schizophrenia who have dangerously seriously violently offended in order to determine the extent to which they shed light on the degree to which the membrane phospholipid hypothesis and the actions of free radicals and other reactive species are associated with cerebral pathophysiological mechanisms in this group of patients.</p> <p>Methods</p> <p>The patients investigated were inpatients from a medium secure unit with a DSM-IV-TR diagnosis of schizophrenia. There was no history of alcohol dependency or any other comorbid psychoactive substance misuse disorder. Expert psychiatric opinion, accepted in court, was that all these patients had violently offended directly as a result of schizophrenia prior to admission. These offences consisted of homicide, attempted murder or wounding with intent to cause grievous bodily harm. Excreted ethane was analyzed and quantified by gas chromatography and mass spectrometry (<it>m</it>/<it>z </it>= 30). 31-phosphorus magnetic resonance spectroscopy data were obtained at a magnetic field strength of 1.5 T using an image-selected <it>in vivo </it>spectroscopy sequence (TR = 10 s; 64 signal averages localized on a 70 × 70 × 70 mm³voxel).</p> <p>Results</p> <p>Compared with age- and sex-matched controls, in the patient group the mean alveolar ethane level was higher (<it>p </it>< 0.0005), the mean cerebral beta-nucleotide triphosphate was lower (<it>p </it>< 0.04) and the mean gamma-nucleotide triphosphate was higher (<it>p </it>< 0.04). There was no significant difference between the two groups in respect of phosphomonoesters, phosphodiesters or broad resonances.</p> <p>Conclusion</p> <p>Our results are not necessarily inconsistent with the membrane phospholipid hypothesis, given that the patients studied suffered predominantly from positive symptoms of schizophrenia. The results suggest that there is increased cerebral mitochondrial oxidative phosphorylation in patients with schizophrenia who have dangerously and seriously violently offended, with an associated increase in oxygen flux and subsequent electron 'leakage' from the electron transport chain leading to the formation of superoxide radicals and other reactive oxygen species. In turn, these reactive species might cause increased lipid peroxidation in neuroglial membranes, thereby accounting for the observation of increased ethane excretion.</p