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

Pannuru Padmavathi1, Vaddi Damodara Reddy, Paramahamsa Maturu

  • 1Department of Biochemistry, Sri Krishnadevaraya University, Anantapur -515 055, AP, India.

Journal of Atherosclerosis and Thrombosis
|February 16, 2010
PubMed

Insights

Cigarette smoking significantly alters platelet membrane properties, increasing the cholesterol-to-phospholipid ratio and reducing fluidity. These changes in smokers are linked to elevated LDL and VLDL cholesterol levels, contributing to cardiovascular risk.

Area of Science:

  • Cardiovascular Science
  • Biochemistry
  • Hematology

Background:

  • Cigarette smoking is a major risk factor for cardiovascular diseases and atherosclerosis.
  • Smoking increases platelet aggregation and modifies hemostatic parameters, leading to higher cardiovascular event rates.
  • Specific effects of smoking on platelet membrane fluidity and composition remain understudied.

Purpose of the Study:

  • To investigate the impact of cigarette smoking on platelet membrane fluidity and lipid composition.
  • To assess alterations in platelet membrane Na(+)/K(+)-ATPase activity and other biochemical markers in smokers.
  • To correlate smoking-induced changes in platelet membranes with plasma lipid profiles.

Main Methods:

  • Studied 30 subjects (experimental smokers and controls), with experimental subjects smoking 10 cigarettes/day for 7-10 years.
  • Determined plasma lipid profiles, platelet carbonyls, sulfhydryl groups, Na(+)/K(+)-ATPase activity, and membrane fluidity using DPH.
  • Analyzed total cholesterol, phospholipids, and individual phospholipids in platelet membranes.

Main Results:

  • Smokers exhibited increased platelet membrane cholesterol-phospholipid ratio, elevated phosphatidylethanolamine and phosphatidylserine, and decreased phosphatidylcholine.
  • Platelet Na(+)/K(+)-ATPase activity and membrane fluidity were reduced in smokers.
  • Smokers showed increased plasma total cholesterol, LDL-cholesterol, and protein carbonyls, with decreased HDL-cholesterol and sulfhydryl groups.

Conclusions:

  • Elevated plasma LDL-cholesterol, VLDL-cholesterol, and total cholesterol likely contribute to the increased cholesterol-phospholipid ratio in smoker's platelets.
  • These lipid alterations may lead to decreased platelet membrane fluidity in cigarette smokers.
  • Findings suggest smoking-induced platelet membrane changes are linked to dyslipidemia, potentially increasing cardiovascular risk.
Abstract

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