Morrow J D, Frei B, Longmire A W, Gaziano J M, Lynch S M, Shyr Y, Strauss W E, Oates J A, Roberts L J
Department of Medicine, Vanderbilt University, Nashville, TN 37232-6602, USA.
N Engl J Med. 1995 May 4;332(18):1198-203. doi: 10.1056/NEJM199505043321804.
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.
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.
Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (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).
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.
据推测，吸烟所致疾病的发病机制涉及自由基引起的氧化损伤。然而，缺乏吸烟在体内导致靶分子氧化修饰的确切证据。我们开展了一项研究，以确定吸烟人群中脂质过氧化的新产物F2 -异前列腺素的生成是否增加。
我们测定了10名年龄和性别匹配的吸烟者及10名不吸烟者血浆中游离F2 -异前列腺素的水平、与血浆脂质酯化的F2 -异前列腺素的水平以及F2 -异前列腺素代谢产物的尿排泄量。我们还测定了吸烟的短期效应（30分钟内吸3支烟）以及吸烟者戒烟两周对循环中F2 -异前列腺素水平的影响。
吸烟者血浆中游离和酯化F2 -异前列腺素的水平（分别为每升242±147和574±217皮摩尔）显著高于不吸烟者（每升103±19和345±65皮摩尔；游离F2 -异前列腺素P = 0.02，酯化F2 -异前列腺素P = 0.03）。吸烟对循环中F2 -异前列腺素的水平无短期影响。然而，戒烟两周后，游离和酯化F2 -异前列腺素的水平显著下降（戒烟前分别为每升250±156和624±214皮摩尔，戒烟两周后分别为每升156±67和469±108皮摩尔；游离F2 -异前列腺素P = 0.03，酯化F2 -异前列腺素P = 0.02）。
吸烟者循环中F2 -异前列腺素水平升高支持了吸烟可在体内导致重要生物分子氧化修饰这一假说。
