Vitamin E and other Lipophilic Antioxidants Protect LDL against Oxidation

Abstract

Abstract Oxidized LDL is taken up by the macrophage scavenger receptor and leads to lipid laden foam cells, which are characteristic constituents of early atheroschlerotic lesions. Oxidation of LDL is a lipid peroxidation process, in which the PUFAs contained in the LDL lipids (on average 1200 molecules PUFAs/LDL particle, 88% 18:2, 12% 20:4) are rapidly converted to lipid hydroperoxides and to aldehydic lipid peroxidation products. Aldehydes and lipid alkoxy radicals alter the property of the apo‐B. The rapid oxidation of LDL is preceded by a lag phase during which the endogeneous antioxidants of LDL are consumed in the sequence: alphatocopherol, gamma‐tocopherol, lycopine, retinyl derivative and betacarotene. LDL with artificially elevated alpha‐tocopherol content is significantly more resistant to oxidation as measured by the duration of the lag phase. Prate and ascorbate can also retard LDL oxidation.