Cellular Catabolism of Serum Lipoproteins
During the past decade, attention has focused on the catabolism of the lipid and protein components of serum lipoproteins. In the rat (Roheim et al., 1971) and probably also in the human, the high-density lipoproteins (HDL) are cleared from the circulation as complete particles. In the rat their half-life in the circulation is about 10 h and the main organ responsible for the removal of serum HDL is the liver (Roheim et al., 1971). With the help of radioautography, it was shown that the labeled protein is taken up by the parenchymal cells. Concentrations of radioautographic reaction over secondary lysosomes pointed to these organelles as the site of HDL catabolism (Rachmilewitz et al., 1972). The degra-tion of serum very low-density lipoproteins proceeds in two stages — vascular and cellular and again the parenchymal cells of the liver were shown to be responsible for the cellular phase (Stein et al., 1974). Radioautography at the electron microscope level revealed that binding of the particles to the sinusoidal cell surface of hepatocytes precedes their interiorization. Concentrations of label found over secondary lysosomes provided support that the degradation of protein moiety of serum VLDL or rather remnant particles (Stein et al., 1974) is effected by lysosomal enzymes. Presently, the effect of chloroquine, an inhibitor of cathepsin B, on the degradation of serum lipoproteins in rat liver was studied in vivo and in liver homogenates.
KeywordsCholesterol Hydrolysis Albumin EDTA Stein
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