ABSTRACT
The results of the atherogenesis experiment are detailed in Table 3. There were no significant differences in weight gain or serum lipids. However, the rabbits fed CLA exhibited 31% less severe atheromata in the aortic arch and a 40% lower severity in the thoracic aorta. After rabbits followed the regression regimen for 90 d, serum cholesterol had fallen by 83% for the control regimen and 67% for the CLA diet. The percentage of HDL-C had risen by 121 and 74%, respectively. Serum TG concentrations were unchanged in the control group but were 58% lower in the CLA-fed rabbits. Examination of the level of atherosclerosis revealed that there had been practically no change in the control rabbits, but severity of atherosclerosis in the aortic arch and thoracic
Introduction Oxidized cholesterol has been found to be atherosclerotic (1) and to cause arterial injury in rabbits (2). Steinberg and his colleagues (3) showed that oxidized low density lipoprotein (LDL) plays a crucial role in atherogenesis. They also reported that a pharmaceutical agent with antioxidant properties, probucol [4,4′(isopropylidenedithio)bis(2,5-di-tbutylphenol)], could prevent oxidation of LDL in vitro and in vivo and also prevent the progression of atherosclerosis in the Watanabe heritable hyperlipidemic (WHHL) rabbit. The action is due to its antioxidant properties and is independent of its hypolipidemic properties (4,5). Earlier, probucol was found to inhibit cholesterol-induced atherosclerosis in rabbits (6). Reports that conjugated linoleic acid (CLA) exhibited antioxidant activity in vivo (7) and in vitro (8) prompted investigation of its effects on atherogenesis in cholesterol-fed rabbits. The CLA used in our studies was a mixture of conjugated dienoic derivatives of linoleic acid, primarily the cis-9, trans-1l, and trans-10, cis-12 isomers.
