Abstract
The amount of α‐tocopherol (α‐TOH) can dramatically alter the extent of radical‐induced oxidation of low density lipoprotein (LDL) lipids, a process generally thought to be important in atherogenesis. However, LDL with atherogenic features can also be formed in vitro by exposure to the strong non‐radical oxidant hypochlorite (HOCl), which preferentially oxidises LDL apolipoprotein B‐100. Here we show that varying LDL content of α‐TOH by vitamin supplementation or depletion has no effect on the extent of HOCl‐induced oxidation of apolipoprotein B‐100 as measured by the loss of lysine and tryptophan residues, and the alteration in relative electrophoretic mobility of the lipoprotein particle.

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