Abstract
The urinary metabolites (Z)-7-[1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]cyclopentyl]hept-5-enoic acid (8-iso-PGF2α), an F2-isoprostane and biomarker of oxidative damage, and “prostaglandin E2 metabolite” (PGE-M), a biomarker of inflammation, are elevated in cigarette smokers. However, there is little information in the literature on the longitudinal stability of these widely used biomarkers. In a large clinical trial involving 10 institutional sites, smokers were given, free of charge over a period of 20 weeks, Spectrum NRC600/601 research cigarettes containing 15.5 mg nicotine/g tobacco. All participants were instructed to smoke these cigarettes for the duration of the study. At weeks 4, 8, 12, 16, and 20, first morning urine voids were collected and analyzed for 8-iso-PGF2α and PGE-M using validated liquid chromatography-electrospray ionization-tandem mass spectrometry methods. The mean level of 8-iso-PGF2α at Week 4 was 1.34 ± 1.08 (S.D.) pmol/mg creatinine (N = 226) while that of PGE-M was 73.7 ± 113 (S.D.) pmol/mg creatinine (N = 232). The corresponding levels at Week 20 were 1.35 ± 0.93 (S.D.) pmol/mg creatinine (N = 209) for 8-iso-PGF2α and 74.2 ± 142 (S.D.) pmol/mg creatinine (N = 210) for PGE-M. There was variation in these values in the intervening weeks. The intra-class correlation coefficients (ICC) were 0.51 (95% CI, 0.45, 0.57) and 0.36 (0.30, 0.43), for 8-iso-PGF2α and PGE-M, respectively, indicating fair longitudinal stability for 8-iso-PGF2α and poorer longitudinal stability for PGE-M in cigarette smokers. Males had higher ICC values than females for both 8-iso-PGF2α and PGE-M. These results indicate that, in addition to cigarette smoking, endogenous processes of oxidative damage and inflammation influence the levels of these biomarkers over time among current smokers.
Highlights
The closely linked phenomena of oxidative damage and inflammation play a significant role in diseases caused by cigarette smoking including cancer, cardiovascular disease, and chronic obstructive pulmonary disease [1, 2]
These results indicate that, in addition to cigarette smoking, endogenous processes of oxidative damage and inflammation influence the levels of these biomarkers over time among current smokers
The analytical chemistry validation data reported here were important for our study of the longitudinal stability of 8-iso-PGF2α and PGE-M
Summary
The closely linked phenomena of oxidative damage and inflammation play a significant role in diseases caused by cigarette smoking including cancer, cardiovascular disease, and chronic obstructive pulmonary disease [1, 2]. Multiple studies have reliably shown that smokers have increased 8-iso-PGF2α in urine compared to non-smokers [6,7,8,9,10,11,12]. Studies have shown that levels of 8-iso-PGF2α decrease upon smoking cessation [13, 15, 16] Together, these data clearly show that cigarette smoking increases levels of 8-iso-PGF2α, indicating oxidative damage. It is important to know the variation in a biomarker over time under relatively constant conditions in order to properly assess the effects of changes in tobacco use on their levels.
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