Evidence that oxidation of LDL renders it more atherogenic has spurred interest in the mechanisms by which LDL oxidation may occur and interventions to slow the rate of oxidation. Release of superoxide anion appears to be a major pathway in cultured smooth muscle cells, fibroblasts and circulating monocytes. Generation of lipoperoxides by the action of 15-lipoxygenase appears to be of major importance in oxidation catalyzed by macrophages and by endothelial cells. Evidence with respect to the role of these mechanisms in vivo is severely limited. While oxidation of LDL almost certainly occurs within the artery wall, it is not known with certainty which cells are most important nor to what extent other tissue sites of LDL oxidation play a role in vivo.
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Parthasarathy et al. (1992) studied this question.