EFFECT OF CIGARETTE-SMOKING ON THE LEVELS OF PLATELET-ACTIVATING FACTOR-LIKE LIPID(S) IN PLASMA-LIPOPROTEINS
EFFECT OF CIGARETTE-SMOKING ON THE LEVELS OF PLATELET-ACTIVATING FACTOR-LIKE LIPID(S) IN PLASMA-LIPOPROTEINS
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DOI：
10.1016/0021-9150(91)90231-q
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发表时间：
1991-03-01
期刊：
影响因子：
5.3
通讯作者：
TAKAMATSU, S
中科院分区：
文献类型：
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作者：
IMAIZUMI, TA;SATOH, K;TAKAMATSU, S
研究吸烟对血浆脂蛋白中血小板活化因子样脂(S)水平的影响。受试者为10名健康男性非吸烟者(24+/-1.4岁)和13名健康男性习惯性吸烟者(23+/-1.3岁)。取空腹静脉血，测定基础血浆脂蛋白中PAF-11水平。吸烟对吸烟者的急性影响也进行了研究。超速离心法分离血浆脂蛋白。用薄层层析法提取和分离脂类。与正品PAF具有相同迁移率的组份被回收，并被证明能引起人多形核中性粒细胞聚集。这种活性被鉴定为PAF-11，因为它被磷脂酶A2灭活，并被PAF受体拮抗剂CV-3988阻断。PAF-11在低密度脂蛋白和高密度脂蛋白中检测到，但在极低密度脂蛋白或脂蛋白缺乏的血浆中未检测到。非吸烟者、吸烟者吸烟前后低密度脂蛋白水平分别为13+/-7.5pg/ml、16+/-14.9pg/ml和190+/-179.0 pg/ml，高密度脂蛋白水平分别为12+/-5.2pg/ml、40+/-40.0 pg/ml和235.0pg/ml。吸烟者吸烟后低密度脂蛋白和高密度脂蛋白水平均显著升高(P<；0.05)。30min后，血药浓度基本恢复到吸烟前水平。结论：吸烟可引起低密度脂蛋白和高密度脂蛋白中PAF或与之密切相关的脂质(S)水平升高，这可能与吸烟诱导的动脉粥样硬化有关。
The effect of cigarette smoking on the levels of platelet-activating factor-like lipid(s) (PAF-LL) in plasma lipoproteins was studied. The subjects were 10 healthy male non-smokers (24 +/- 1.4 years old) and 13 healthy male habitual smokers (23 +/- 1.3 years old). Fasting venous blood was obtained and basal levels of PAF-LL in plasma lipoproteins were estimated. The acute effect of cigarette smoking was also studied in smokers. Plasma lipoproteins were separated by ultracentrifugation. Lipids were extracted and separated by thin-layer chromatography. The fraction with the same migration as authentic PAF was recovered and was shown to cause aggregation of human polymorphonuclear neutrophils. This activity was identified as PAF-LL because it was inactivated by phospholipase A2 and was blocked by CV-3988, an antagonist of the PAF receptor. PAF-LL was detected in LDL and HDL, but not in VLDL or in lipoprotein-deficient plasma. The levels of PAF-LL in LDL in non-smokers, and in smokers before and after smoking were 13 +/- 7.5, 16 +/- 14.9 and 190 +/- 179.0 pg/ml, and those in HDL were 12 +/- 5.2, 40 +/- 40.0 and 235 +/- 205.1 pg/ml, respectively. The values in both LDL and HDL in smokers increased significantly after smoking (P < 0.05). After 30 min, the levels had returned almost to the pre-smoking levels. We conclude that cigarette smoking induces an increase in the levels of PAF or closely related lipid(s) in LDL and HDL, which may be related to smoking-induced atherosclerosis.