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Treatment of Cholesterol-Fed Rabbits with Dietary Vitamins E and C Inhibits Lipoprotein Oxidation but Not Development of Atherosclerosis^1,2,

Diane W. Morel^*,,3, Margarita de la Llera-Moya and Karen E. Friday^{*,, ,4}

^* Division of Nutrition Department of Biochemistry Department of Medicine, Medical College of Pennsylvania, Philadelphia, PA 19129

New Zealand White rabbits were made hypercholesterolemic by feeding a high cholesterol diet (10 g/kg diet) with or without added antioxidants. The antioxidants used were either probucol (10 g/kg) or vitamin E (10 g/kg) plus vitamin C (0.6 g/kg). Serum cholesterol concentrations were monitored as a function of time. At the end of 10 wk, serum and lipoprotein vitamin E concentrations, the extent of oxidation of lipoprotein fractions (thiobarbituric acid reacting substances), the susceptibility of lipoprotein to oxidation in vitro (conjugated diene formation) and the extent of atherosclerosis (aortic area stained by Sudan IV and plaque thickness) were measured. Rabbits fed diets supplemented with vitamins E and C had markedly higher serum vitamin E concentrations, marked vitamin E enrichment in all lipoprotein fractions, less oxidation in VLDL and LDL and enhanced resistance of LDL to further in vitro oxidation, but did not have significantly less aortic atherosclerosis. Rabbits given supplemental probucol likewise exhibited reduced oxidation of lipoproteins. However, aortic atherosclerosis in these animals was significantly lower, as were serum cholesterol concentrations. Inhibition of lipoprotein oxidation itself was not sufficient to reduce atherosclerosis in cholesterol-fed New Zealand White rabbits.

KEY WORDS: • atherosclerosis • lipoprotein oxidation • antioxidants • cholesterol • rabbits

¹ These studies were funded in part by a Ciba-Geigy Intramural Clinical Pharmacology Research Award (K.E.F.), an NIH FIRST Award (HL-44306, D.W.M.), a Johnson and Johnson Focussed Giving Program Grant (M.L.M.) and the Howard Heinz Endowment.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence should be addressed.

⁴ Current address: Department of Medicine, Tulane Medical School, New Orleans, LA.

Manuscript received 28 December 1993. Revision accepted 9 March 1994.