Abstract

Oxidation of human low-density lipoprotein (LDL) is implicated as an initiator of atherosclerosis. α-Tocopherol (α-TocH) may thus inhibit atherosclerosis beause it is the major and most active chain-breaking antioxidant in extracted LDL lipid. Our studies show, however, that α-TocH can be a strong prooxidant for the LDL itself, i.e., an aqueous dispersion of lipid-bearing particles. Thus, a steady flux (R g ) of alkylperoxyl radicals (ROO . ) generated from a water-soluble azo initiator induced lipid peroxidation in LDL which was faster in the presence of α-TocH than in its absence (for R g <2 NM S -1 ), insensitive to R g and [O 2 ], and inhibited by vitamin C, ubiquinol-10 (normally present in fresh LDL), and small phenolic antioxidants but not inhibited by the aqueous radical scavenger uric acid

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