Abstract
Vitamin E deficiency in two species of monkeys (capuchins and cynamolgus) reduced the in vitro cholesterol esterification by plasma lecithin-cholesterol acyltransferase. The reduction was greates in the most deficient species and in animals fed a diet rich in polyunsaturated fat (safflower oil) stripped of vitamin E. The best correlate of total esterification was the plasma concentration of free cholesterol which reflected the degree of hyperlipidemia, found to be greatest in capuchins fed coconut oil. A logical explanation for the decreased LCAT activity in vitamin E deficiency would be peroxidative damage of substrate (the PUFA of lecithin) or of sulfhydryl sited on lecithin-cholesterol acyltransferase itself. However, neither case was fully supported by the data suggesting that additional information concerning the nature of the reaction and the role of vitamin E is required.