We examined whether oxidized lipids in the diet determine the levels of oxidized lipid in human postprandial serum chylomicrons. After we fed subjects control corn oil containing low quantities of oxidized lipid, the levels of conjugated dienes in the chylomicron fraction were low (9.67 ±0.92 nmol//imol triglyceride), and no thiobarbituric acid-reactive substances (TBARS) could be detected. However, when subjects were fed a highly oxidized oil, the conjugated diene content in chylomicrons was increased 4.7-fold to 46±5.63 nmo\/fimo\ triglyceride, with 0.140±0.03 nmol TBARS//imol triglyceride. When subjects were fed mediumoxidized oil, the degree of oxidation of the chylomicron lipids was moderately increased (21.86 ±2.03 nmol conjugated

Abstract-Oxidized lipoproteins may play a role in atherosclerosis. Recently, we have demonstrated that the levels of oxidized fatty acids in the circulation correlate directly with the quantity of oxidized fatty acids in the diet and that dietary oxidized fatty acids accelerate atherosclerosis in rabbits. The present study tests the hypothesis that oxidized cholesterol in the diet accelerates the development of atherosclerosis. Rabbits were fed a diet containing 0.33% nonoxidized cholesterol (control diet) or the same diet containing 0.33% cholesterol of which 5% was oxidized (oxidized diet). Serum cholesterol levels increased to a similar extent in both groups, with the majority of cholesterol in the ␤-VLDL fraction. Moreover, in the serum ␤-VLDL fraction and liver, there was a significant increase in the oxidized cholesterol levels. Most importantly, feeding a diet enriched in oxidized cholesterol resulted in a 100% increase in fatty streak lesions in the aorta. Western diets contain high concentrations of oxidized cholesterol products, and our results suggest that these foods may be a risk factor for atherosclerosis. (Arterioscler Thromb Vasc Biol. 1998;18:977-983.)

Abstract-The aim of the current study was to determine whether oxidized cholesterol in the diet accelerates atherosclerosis in low density lipoprotein receptor-(LDLR) and apolipoprotein E-(apo E) deficient mice. Mice were fed either a control diet or a diet containing oxidized cholesterol. For LDLR-deficient mice, the control diet consisted of regular mouse chow to which 1.0% cholesterol was added. The oxidized diet was identical to the control diet except that 5% of the added cholesterol was oxidized. In apo E-deficient mice, the control diet contained 0.15% cholesterol, whereas in the oxidized diet, 5% of the added cholesterol was oxidized. LDLR-deficient and apo E-deficient mice were fed the experimental diets for 7 and 4 months, respectively. In mice fed the oxidized-cholesterol diets, the levels of oxidized cholesterol in sera were increased. At the end of the experiment, aortas were removed and atherosclerosis was assessed. We found that in LDLR-deficient mice, feeding of an oxidized-cholesterol diet resulted in a 32% increase in fatty streak lesions (