RELATIVE RESISTANCE OF THE HAMSTER TO AORTIC ATHEROSCLEROSIS IN SPITEOF PROLONGED VITAMIN-E-DEFICIENCY AND DIETARY HYPERCHOLESTEROLEMIA - PUTATIVE EFFECT OF INCREASED HDL

Male golden hamsters were rendered hypercholesterolemic by feeding die ts enriched with cholesterol and fat, In the first series of experimen ts, 5% butter and 1% cholesterol were added to a chow diet and plasma cholesterol levels were maintained at 350-390 mg/dl over the entire ex perimental period. Groups of hamsters and their age controls consuming the chow diet, were killed after 7, 15 and 20 months when the aorta w as examined for atherosclerosis by determination of cholesterol mass. In the controls, aortic total cholesterol (TC) increased with age by 2 8% and esterified cholesterol increased to 11% of TC. In the hyperchol esterolemic animals aortic TC was only 28% higher than in the controls and cholesteryl ester was also 11.5% of TC, In the second series, one group of hamsters were fed a semi-purified diet deficient in vitamin E, containing 1% cholesterol and 10% lard; a second group received the same diet, but supplemented with vitamin E. Controls consumed local c how. After 7 months on the vitamin E deficient diet plasma alpha-tocop herol was 0.05 mg/l, in those supplemented with vitamin E it was 20 mg /l, while in the controls it was 3.3 mg/l. Plasma thiobarbituric acid reactive substances (TEARS) were higher in the vitamin E deficient gro up and then was a greater propensity of lipoproteins (d < 1.063 g/ml) to peroxidation in vitro than in the vitamin E supplemented group. Pla sma cholesterol was 366 mg/dl in the vitamin E deficient, 336 mg/dl in the vitamin E supplemented group, and 64 mg/dl in controls. Aortic ch olesterol was 79.1 in vitamin E supplemented and 84.4 mu g/10 mg dry w eight in vitamin E deficient hamsters. In both series of experiments, HDL amounted to 36-41% of plasma TC in the hypercholesterolemic animal s and 59-62% in the controls. In conclusion: the hamster appears to be quite resistant to atherosclerosis in face of sustained hypercholeste rolemia, even in the presence of increased peroxidative stress caused by vitamin E deficiency. This relative resistance could be related to commensurate increase in plasma HDL which was observed in both series of experiments. Since vitamin E deficiency did not enhance aortic chol esteryl ester deposition, the protective effect of HDL seems to be rel ated to its role in reverse cholesterol transport, rather than in prev ention of peroxidation.