INCREASE IN CIRCULATING PRODUCTS OF LIPID-PEROXIDATION (F-2-ISOPROSTANES) IN SMOKERS - SMOKING AS A CAUSE OF OXIDATIVE DAMAGE
INCREASE IN CIRCULATING PRODUCTS OF LIPID-PEROXIDATION (F-2-ISOPROSTANES) IN SMOKERS - SMOKING AS A CAUSE OF OXIDATIVE DAMAGE
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DOI：
10.1056/nejm199505043321804
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发表时间：
1995-05-04
影响因子：
158.5
通讯作者：
ROBERTS, LJ
中科院分区：
文献类型：
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作者：
MORROW, JD;FREI, B;ROBERTS, LJ
背景。据推测，吸烟引起的疾病的发病机制与自由基的氧化损伤有关。然而，明确的证据表明，吸烟导致体内靶分子的氧化修饰是缺乏的。我们进行了一项研究，以确定f -2-异前列腺素（一种脂质过氧化的新产物）的产生是否会在吸烟的人中增加。我们测量了10名吸烟者和10名年龄和性别相匹配的非吸烟者血浆中游离f -2-异前列腺素的水平，f -2-异前列腺素酯化成血浆脂质的水平，以及f -2-异前列腺素代谢产物的尿排泄。吸烟的短期影响（30分钟内抽三支烟）和戒烟两周对吸烟者血液循环中f -2异前列腺素水平的影响也被确定。吸烟者血浆游离和酯化的f -2异前列腺素水平（平均+/-SD， 242+/-147和574+/-217 pmol / l）显著高于非吸烟者（103+/-19和345+/-65 pmol / l；游离f -2异前列腺素水平P = 0.02，酯化f -2异前列腺素水平P = 0.03）。吸烟对循环中的f -2异前列腺素水平没有短期影响。然而，戒烟两周后，游离和酯化的f -2-异前列腺素水平显著下降（戒烟前分别为250+/-156和624+/-214 pmol / l，戒烟两周后分别为156+/-67和469+/-108 pmol / l；游离f -2-异前列腺素水平P=0.03，酯化f -2-异前列腺素水平P= 0.02）。吸烟者血液循环中f -2-异前列腺素水平的增加支持了吸烟可引起体内重要生物分子氧化修饰的假设。
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 F-2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke.Methods. We measured the levels of free F-2-isoprostanes in plasma, the levels of F-2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F-2-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 F-2-isoprostanes in the circulation were also determined in the smokers.Results. Plasma levels of free and esterified F-2-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 F-2-isoprostanes and P = 0.03 for esterified F-2-isoprostanes). Smoking had no short-term effects on the circulating levels of F-2-isoprostanes. However, the levels of free and esterified F-2-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 F-2-isoprostanes and P = 0.02 for esterified F-2-isoprostanes).Conclusions. The increased levels of F-2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.