Chapter 11. Cholesterol Exchange Between Surface Layers and Plasma Proteins in bulk

  1. Ruth Porter and
  2. Julie Knight
  1. I. R. Miller,
  2. H. Graet and
  3. Y. F. Frei

Published Online: 30 MAY 2008

DOI: 10.1002/9780470719954.ch11

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

How to Cite

Miller, I. R., Graet, H. and Frei, Y. F. (1973) Cholesterol Exchange Between Surface Layers and Plasma Proteins in bulk, in Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors (eds R. Porter and J. Knight), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470719954.ch11

Author Information

  1. Polymer Department, Weitzman Institute of Science, Rehoboth, Israel

Publication History

  1. Published Online: 30 MAY 2008
  2. Published Print: 1 JAN 1973

ISBN Information

Print ISBN: 9789021940137

Online ISBN: 9780470719954



  • plasma proteins;
  • cholesterol exchange;
  • protein concentration;
  • lipoproteins;
  • blood vessels


3H-Labelled cholesterol and delipidized low-density β-lipoproteins have been used to elucidate the exchange mechanism operating in a model system. The rate of dissolution of 3H-labelled cholesterol monolayers by whole plasma and by lipoprotein fractions has been investigated by measuring the changes in radioactivity in the surface and bulk phases. The rate of dissolution was slow, and increased with the protein concentration, approaching a constant rate of about 5 % of the monolayer per hour at high protein concentrations. Vigorous stirring produces an unstable dispersion of the cholesterol in the bulk solution, which reforms as a surface layer within less than an hour.

Using radioactively labelled proteins, formed by acetylation with [3H]acetic anhydride, we found that the proteins form an extremely slowly exchangeable monolayer at the air/water or cholesterol/water interface and a somewhat more readily exchangeable subsequent surface layer. It is concluded that, in order to be solubilized, cholesterol has to diffuse through such a non-desorbable protein monolayer to be bound by the readily exchangeable lipoprotein molecules.

In the light of these findings and of the results obtained for the shear rate dependent accumulation of cholesterol in artery walls in atheroma formation, the following working hypothesis is suggested. Lipoproteins are only weakly absorbed on young proteinaceous blood vessels. In regions of low shear rate the lipoproteins adhering to the wall may undergo metabolic changes, leaving behind an excess of lipids. This makes the surface increasingly hydrophobic and thus enhances the further adsorption of lipoprotein molecules. Higher shear rates oppose and may even reverse this process.