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吸烟导致慢性吸烟者血小板膜流动性和 Na(+)/K(+)-ATP 酶活性改变。

Smoking-induced alterations in platelet membrane fluidity and Na(+)/K(+)-ATPase activity in chronic cigarette smokers.

机构信息

Department of Biochemistry, Sri Krishnadevaraya University, Anantapur -515 055, AP, India.

出版信息

J Atheroscler Thromb. 2010 Jun 30;17(6):619-27. doi: 10.5551/jat.2857. Epub 2010 Feb 13.

Abstract

AIM

Cigarette smoking is a recognized risk factor for cardiovascular diseases and has been implicated in the pathogenesis of atherosclerosis. Platelet adhesiveness and aggregation increases as a result of smoking. Cigarette smoking modifies haemostatic parameters via thrombosis with a consequently higher rate of cardiovascular events, but smoking-induced alterations of platelet membrane fluidity and other changes have not been studied.

METHODS

Thirty experimental and control subjects (mean age 35+/-8) were selected for the study. Experimental subjects had smoked 10+/-2 cigarettes per day for 7-10 years. The plasma lipid profile, platelet carbonyls, sulfhydryl groups, Na(+)/k(+)-ATPase activity, fluidity using a fluorescent probe 1,6-diphenyl-1,3,5-hexatriene (DPH), total cholesterol and phospholipids as well individual phospholipids were determined.

RESULTS

Increases in the platelet membrane cholesterol phospholipid (C/P) ratio, phosphotidylethanolamine, phosphotidylserine with decreased phosphotidylcholine, Na(+)/k(+)-ATPase activity, fluidity and no significant change in phosphotidylinositol and sphingomylein, as well as increases in plasma total cholesterol, LDL-cholesterol, protein carbonyls with decreased HDL-cholesterol and sulfhydryl groups were observed in cigarette smokers. Platelet membrane total phospholipids were positively correlated with plasma LDL-cholesterol (r=0.568) and VLDL-cholesterol (r=0.614) in cigarette smokers.

CONCLUSIONS

Increased plasma LDL-cholesterol, VLDL-cholesterol and total cholesterol might have resulted in the increased C/P ratio and decreased platelet membrane fluidity of cigarette smokers.

摘要

目的

吸烟是心血管疾病的公认危险因素,并与动脉粥样硬化的发病机制有关。吸烟会导致血小板黏附和聚集增加。由于血栓形成,吸烟会改变止血参数,从而导致心血管事件的发生率更高,但吸烟对血小板膜流动性和其他变化的影响尚未得到研究。

方法

选择 30 名实验和对照受试者(平均年龄 35+/-8 岁)进行研究。实验组每天吸烟 10+/-2 支,吸烟时间为 7-10 年。测定了血浆脂质谱、血小板羰基、巯基、Na(+)/k(+)-ATP 酶活性、使用荧光探针 1,6-二苯基-1,3,5-己三烯(DPH)测定的血小板膜流动性、总胆固醇和磷脂以及各个磷脂。

结果

吸烟组血小板膜胆固醇/磷脂(C/P)比值增加,磷酸乙醇胺、磷酸丝氨酸增加,而磷酸胆碱减少,Na(+)/k(+)-ATP 酶活性、流动性降低,磷酸肌醇和神经鞘磷脂无明显变化,血浆总胆固醇、LDL-胆固醇、蛋白羰基增加,HDL-胆固醇和巯基减少。吸烟组血小板膜总磷脂与血浆 LDL-胆固醇(r=0.568)和 VLDL-胆固醇(r=0.614)呈正相关。

结论

血浆 LDL-胆固醇、VLDL-胆固醇和总胆固醇的增加可能导致吸烟组 C/P 比值增加和血小板膜流动性降低。

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