Esterification of cholesterol by homogenates of atherosclerotic and normal aortas

Abstract

Cholesterol esterification with palmityl-CoA by cell-free homogenates from atherosclerotic rabbit aortas was 39 times greater than with cell-free homogenates from normal aortas. In a 2 1 2 hr time-trend study using atherosclerotic preparations, the specific activity curve of cholesteryl ester reached an early plateau at a level much lower than that of the fatty acid derived from the β-position of lecithin, with no tendency of the cholesteryl ester specific activity to rise further approaching that of lecithin. A similar type of experiment was done using normal aortic preparations. In contrast to the experiments with atherosclerotic tissue, the specific activity of cholesteryl ester was much higher than that of lecithin at each time interval after 4 minutes of incubation. The data indicate that lecithin is not an intermediate in the observed esterification of cholesterol in our preparations. Esterification of cholestrol occurs upon addition of labeled palmityl-CoA, and terminates after exhaustion of the substrate. Most of the cholesterol-esterifying activity is localized in the microsomes of normal and atherosclerotic aortas. Cholesterol esterification by atherosclerotic and normal microsomes requires ATP and CoA, when free fatty acid is provided as the acyl source. Very little esterification occurs without these factors. These observations together indicate that cholesterol esterification is accomplished by fatty acyl-CoA:cholesterol acyltransferase.