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Clinical Science (2008) Immediate Publication, doi:10.1042/CS20070404

The association between both lipid and protein oxidation and the risk of fatal or non-fatal coronary heart disease in a human population
Mark Woodward, Kevin D Croft, Trevor A Mori, Henrietta Headlam, Xiao S Wang, Cacang Suarna, Mark J Raftery, Stephen W MacMahon and Roland Stocker

Medicine, Mount Sinai Medical Center, New York, NY 10029, U.S.A.. mark.woodward@mountsinai.org

Background: The role of oxidative damage in the etiology of coronary disease remains controversial; clinical trials investigating the effect of antioxidants have not generally been positive. Methods and Results: 227 coronary cases, identified from a cohort study, were matched, by age and sex, with 420 controls in a nested case-control design. Stored plasma samples were analyzed for F2-isoprostanes by stable isotope dilution mass spectrometry, and specifically oxidized forms of apolipoprotein A I by high performance liquid chromatography analysis of high-density lipoprotein. Median values of F2-isoprostanes were higher in plasma samples that contained oxidized apolipoprotein A I compared to samples with undetectable oxidized apolipoprotein A I (1542 v 1165 pmol/L). F2-isoprostanes were significantly correlated with variants of non-oxidized apolipoprotein A II (r=-0.15) and were associated with high-density lipoprotein cholesterol (p<0.0001). F2-isoprostanes in cases (median, 1146 pmol/L) were not different from controls (1250 pmol/L); the odds ratio (95% confidence interval) for a one standard deviation increase in F2-isoprostanes was 1.08 (0.91-1.29). Similarly, there was no independent association between the presence of oxidized apolipoprotein A I, detected in ~20% of the samples, and coronary risk. Conclusions: We found no evidence of associations between markers of lipid (F2-isoprostanes) and protein (oxidized apolipoprotein A I) oxidation and the risk of fatal or non-fatal coronary heart disease in a general population. This may be due to true lack of association or insufficient power.
doi:10.1042/CS20070404
Received 16 November 2007/12 May 2008; Accepted 28 May 2008
Published as Immediate Publication 28 May 2008



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