Tissue uptake of biologically modified low density lipoprotein in the rat

Abstract

Human low density lipoprotein (LDL) was modified by exposure to cultured human endothelial cells. The endothelial cell modified LDL (EC-LDL) and control LDL (con LDL) labelled with ¹²⁵I-tyramincellobiose (¹²⁵I-TC) were injected into rats. Since ¹²⁵I-TC is trapped in lysosomes the contribution of various organs to the catabolism of EC-LDL and con LDL could be studied. First, EC-LDL was cleared from plasma several times faster than con LDL. Then, the liver was found to be the major organ for catabolism of EC-LDL. Con LDL was distributed more evenly among the spleen, liver and adrenals as the main organs. In the liver the endothelial cells were most effective in degrading EC-LDL whereas con LDL was distributed approximately evenly between the Kupffer, endothelial and parenchymal cells. Thus, the liver endothelial cells seem to be a major pathway for catabolism of modified LDL.

Key words:

• arteriosclerosis
• endothelial cells
• low density lipoprotein
• macrophages