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It has been suggested that macrophages in atherosclerotic plaques oxidize the lipid they contain, leading to necrosis in the plaque. Over 200 human aortic and coronary atherosclerotic plaques from 102 human necropsy subjects aged between 5 and 88 were, therefore, examined histologically for the presence of insoluble lipid (ceroid), thought to be a product of lipid oxidation. Ceroid was present in all the plaques but not in areas of diffuse intimal thickening. In early lesions the insoluble lipid was within membrane-bound vesicles in macrophage-like cells, many showing characteristic ring structures suggesting that membrane-associated oxidative systems might be responsible for rendering the lipid insoluble. Staining was increased by an oxidizing agent and abolished by a reducing agent. It is suggested that this distribution supports the concept of lipid oxidation by macrophages within the plaque.
Mitchinson et al. (1985) studied this question.