Metabolic fate of low density lipoprotein and high density lipoprotein labeled with an ether analogue of cholesteryl ester.

Low density lipoprotein (LDL) metabolism by human skin fibroblasts was studied using LDL labeled with a nonhydrolyzable cholesteryl ether analogue, 3H-cholesteryl linoleyl ether (CLE). The 3H-CLE-LDL was taken up by the apo-B, E receptor mediated endocytosis similar to 125I-labeled LDL. This was shown by saturation kinetics of uptake with respect to 3H-CLE-LDL concentration and very low uptake of 3H-CLE-LDL by receptor negative cell strains. When injected (CE)-LDL were cleared at equal rates and about 30% of the injected LDL was recovered in the liver. Treatment with ethinyl estradiol resulted in a three-fold increase in 3H-CLE-LDL uptake by the liver. The liver is also the major site of uptake of 3H-CLE-high density lipoprotein (HDL) (40%-45% of the injected dose) but its uptake by the liver increased only by 20% with estradiol treatment. As 3H-CLE-HDL was cleared from the circulation at a somewhat faster rate than 125I-HDL it appeared that some dissociation in the tissue uptake of the protein and CE moieties occurs.