The Role of Oxidative Modification and Antioxidants in LDL Metabolism and Atherosclerosis

  • Wendy Jessup
  • Roger T. Dean
  • Catherine V. de Whalley
  • Sara M. Rankin
  • David S. Leake
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 264)


Recent studies have shown that low-density lipoprotein (LDL), when incubated with certain cell types in culture (including endothelial cells, smooth muscle cells and macrophages) is subject to a number of alterations in its physical and chemical properties1. Most interestingly, this ‘modified’ LDL is endocytosed by macrophages up to 20 times more rapidly than native LDL1,2. It is possible that the formation of foam cells from macrophages in the developing atherosclerotic plaque could be the result of the generation of similar ‘modified’ LDL particles by cells of the artery wall. Because the route for endocytosis of ‘modified’ LDL largely bypasses the normal ApoB/E receptor, target cells such as the macrophage are unable to regulate their intake of this ligand and so accumulate large amounts of cholesteryl esters intracellularly.


Cholesteryl Ester Oxidative Modification Endogenous Antioxidant Tocopherol Level Iodine Monochloride 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Heinecke, J.W. (1987) Free Radical Biol. Med. 3, 65–73.CrossRefGoogle Scholar
  2. 2.
    Rankin, S.M., Leake, D.S. (1988) Agents Actions Suppl. 26 ,233-239.Google Scholar
  3. 3.
    Esterbauer, H., Jurgens, G., Quehenberger, O., Koller, E. (1987) J. Lipid Res. ¿8, 495–620.Google Scholar
  4. 4.
    Esterbauer, H., Striegl, G., Puhl, H., Rotheneder, M. (1989) Free Rad. Res. Comms., in press.Google Scholar
  5. 5.
    Havel, R.J., Eder, H.H., Bragdon, J.H. (1955) J. Clin. Invest. 34, 1345– 53.PubMedCrossRefGoogle Scholar
  6. 6.
    Bilheimer, D.W.S., Eisenberg, S., Levy, R.I. (1972) Biochim. Biophys. Acta 60, 212–221.Google Scholar
  7. 7.
    Willson, R.L. (1978) In: Biochemical mechanisms of liver injury. (Slater, T.F.; Ed.) pp.123–224, Academic Press, N.Y.Google Scholar
  8. 8.
    Burton, G.W., Webb, A, Ingold, K.U. (1985) Lipids 20, 29–39.PubMedCrossRefGoogle Scholar
  9. 9.
    Thomas, S.M., Jessup, W., Gebicki, J.M., Dean, R.T. (1989) Anal. Biochem. 176, 353–359.PubMedCrossRefGoogle Scholar
  10. 10.
    Gebicki, J.M., Bielski, B.H.J. (1981) J. Am. Chem. Soc. 103, 7020–7022.CrossRefGoogle Scholar
  11. 11.
    Rankin, S.M., Hoult, J.R.S., Leake, D.S. (1988) Brit. J. Pharmacol, in press.Google Scholar
  12. 12.
    Rankin, S.M., Hoult, J.R.S., Leake, D.S. (1988) Proc. 4th Int. Atherosclerosis Conf., Rome,; in press.Google Scholar
  13. 13.
    Gey, F. (1986) Biblthca Nutr. Dieta. 37 ,53–91.Google Scholar
  14. 14.
    Frei, B., Stocker, R., Ames, B.N. (1988) Proc. Natl. Acad. Sci. USA 85, in press.Google Scholar

Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Wendy Jessup
    • 1
  • Roger T. Dean
    • 2
  • Catherine V. de Whalley
    • 3
  • Sara M. Rankin
    • 3
  • David S. Leake
    • 3
  1. 1.Cell Biology Research GroupBrunei UniversityUxbridgeUK
  2. 2.Heart Research InstituteSydneyAustralia
  3. 3.Department of PharmacologyKing’s College LondonLondonUK

Personalised recommendations