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Previous Volume 332:1198-1203 May 4, 1995 Number 18 Next

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ABSTRACT

Background It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F₂-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke.

Methods We measured the levels of free F₂-isoprostanes in plasma, the levels of F₂-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F₂-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F₂-isoprostanes in the circulation were also determined in the smokers.

Results Plasma levels of free and esterified F₂-isoprostanes were significantly higher in the smokers (mean ±SD, 242±147 and 574±217 pmol per liter, respectively) than in the nonsmokers (103±19 and 345±65 pmol per liter; P = 0.02 for free F₂-isoprostanes and P = 0.03 for esterified F₂-isoprostanes). Smoking had no short-term effects on the circulating levels of F₂-isoprostanes. However, the levels of free and esterified F₂-isoprostanes fell significantly after two weeks of abstinence from smoking (250±156 and 624±214 pmol per liter, respectively, before the cessation of smoking, as compared with 156±67 and 469±108 pmol per liter after two weeks' cessation; P = 0.03 for free F₂-isoprostanes and P = 0.02 for esterified F₂-isoprostanes).

Conclusions The increased levels of F₂-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.

Source Information

From the Departments of Medicine and Pharmacology (J.D.M., A.W.L., J.A.O., L.J.R.) and the Division of Biostatistics, Department of Preventive Medicine (Y.S.), Vanderbilt University, Nashville; the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston (B.F., S.M.L.); the Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston (J.M.G.); and the Section of Cardiology, Brockton–West Roxbury Veterans Affairs Medical Center and Harvard Medical School, Boston (W.E.S.).

Address reprint requests to Dr. Morrow at the Departments of Pharmacology and Medicine, 506 MRB, Vanderbilt University, Nashville, TN 37232-6602.

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