Lipid Peroxidation and atherosclerosis

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Abstract
Atherosclerosis and its clinical sequelae are among the most important of human cardiovascular diseases. Abnormal amounts of lipid are usually present in the thickened intima of atherosclerotic arteries. The notion that lipid peroxidation and polymerization occur in these lipid deposits is based largely on the fact that ceroid pigments have been demonstrated in atherosclerotic plaques. The detection of cholesteryl hydroxyoctadecadienoic acids in lipids of atheromas is suggestive evidence of lipoperoxidation; detection of lipoperoxides as such is technically difficult and the results to date are inconclusive. Studies of arteries from man and animals indicate that ceroid pigments occur late in the disease process and are not likely to be initiators of atherosclerosis. It is possible that hydroperoxides or intermediate free radiclals participate in the early stages of atherogenesis, but this theory is without conclusive support. Ceroid has been implicated as an inflammatory or sclerosing agent in arteries, possibly contributing to the irreversibility of atherosclerosis; confirmation and extension of this observation is needed. There have been no properly controlled studies to evaluate the role of antioxidants in human atherosclerosis as such. Likewise, data from animal experiments concerning the role of alpha‐tocopherol in atherogenesis are inconclusive. We have presented preliminary data showing an inhibitory effect of large amounts of dietary alpha‐tocopherol (1%) on atherogenesis in rabbits fed small amounts (0.5%) of cholesterol. The recent observations that autoxidation products of cholesterol are angiotixic in animals suggest yet another risk factor in human atherogenesis. There is as yet no direct evidence that autoxidation products in human foods pose a serious threat to man, but the preliminary studies in animals suggest the need for further investigation of this possibility.