CONSUMPTION OF EGGS WITH MEALS INCREASES THE SUSCEPTIBILITY OF HUMAN PLASMA AND LOW-DENSITY-LIPOPROTEIN TO LIPID-PEROXIDATION

Consumption of eggs for a long period was shown to result in hyperchol esterolemia and is generally restricted for this reason. In the presen t study we analyzed the effect of eggs consumption for 3 weeks on lipo protein atherogenicity. Consumption of 2 eggs per day with the meals, for 3 weeks resulted in a minor elevation in plasma glucose and urea c oncentrations. Plasma cholesterol concentration increased by 11% (p < 0.05) as a result of increased plasma low-density lipoprotein (LDL) ch oesterol, levels. Plasma triglycerides decreased by 13% (p < 0.01), bu t there were no significant alterations in plasma apolipoproteins A-I or B-100 concentrations. Plasma high-density lipoprotein (HDL) cholest erol decreased by 11% (p < 0.05). There was a 13% reduction, though no t significant, in the cholesterol efflux from J-774 A.1 macrophages by HDL that was derived after eggs consumption in comparison to HDL that was obtained at baseline. The susceptibility of plasma [using 100 mM of 2,2' azobis 2-amidinopropane (APH)] as well as that of LDL (using 1 0 mu M of copper ions) to lipid peroxidation was increased by 42% and 34%, respectively, as measured by the thiobarbituric acid reactive sub stance (TEARS) assay (p < 0.01). Kinetic analysis of LDL oxidation by copper ions revealed a 37% reduction in the lag time required for the initiation of LDL oxidation after 3 weeks of eggs consumption. The tot al plasma fatty acids concentration increased from 2.2 +/- 0.5 to 3.2 +/- 0.6 mg/ml. The plasma antioxidants, vitamin E and carotenoids were not significantly affected by eggs consumption. We conclude that eggs consumption, in addition to its hypercholesterolemic effect, increase s plasma and LDL oxidizability, a phenomenon which was shown to enhanc e the progression of atherosclerosis. These atherogenic properties may contribute to the accelerated atherosclerosis prevalent in population s with high cholesterol intake.