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When exposed to Ct?', a-tocopherol, in detergent dispersion, is rapidly oxidised. Moreover, if phospholipids and traces of their hydroperoxide derivatives are included in these dispersions, Cu" initiates lipid peroxidation, the rate of which is dramatically stimulated by a-tocopherol. The observation that the rate of a-tocopherol consumption is identical in the absence and in the presence of lipids undergoing peroxidation, apparently rules out any antioxidant effect. These results are consistent with a prooxidant effect of vitamin E, mediated by its capability to reduce Cu*+ to Cu' which, in turn, produces, from lipid hydroperoxides, the highly reactive alkoxyl radicals. Present data highlight the risk of misleading results in interpreting the significance of lags in peroxidation of LDL challenged with Cu*'.

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