抄録
To clarify the mechanism of cholesterol ester deposition in the arterial wall, the reconstructed LDL (rLDL) and acetylated LDL (acLDL) cholesterol ester metabolism in the rat peritoneal macrophage and the arterial wall were studied. Reconstructed LDL was prepared by the method of Krieger et al. It is reported that there are acid (pH 4.5) and neutral pH 7.5) cholesterol esterase (CEase) in the arterial wall. rLDL-cholesterol oleate and acLDL-cholesterol oleate were hydrolized by rat arterial homogenate and by rat peritoneal macrophage homogenate only at pH 4.5. Next, microsomal resterification system of cholesterol which was product hydrolized in lysosome was studied. ReLDL[3H]-cholesterol oleate were at first incubated with particulate fractions of arterial wall homogenate or macrophage homogenate at pH 4.5, then were incubated at pH7.5 with the addition of [14C]oleoyl-CoA, and formed amount of [3H]cholesterol-[14C] oleate were measure after separating with thin layer chromatography. The rate of reesterification of cholesterol was enchanced by the addition of supernatant fraction with the arterial wall, but with peritoneal mecrophage, it was decreased by the addition of supernatant fraction. These results suggested that LDL-cholesterol ester metabolism was greatly affected by the factor contained in the supernatant fractions. The hydrolysis of reLDL-cholesterol oleate by both arterial and macrophage homogenate at pH 4.5, was enhanced by the addition of tocopherol. Farther more, tocopheroltreated reLDL cholesterol oleate was much more hydrolized by arterial homogenate or by macrophage homogenate than nontreated reLDL cholesterol oleate, and also tocopherol-treated arterial wall homogenate or macrophage homogenate hydrolized reLDL-cholesterol oleate much more than untreated homogenates. On the other hand, reesterification of once hydrolized reLDL cholesterol by tocopherol-treated arterial wall and macrophage homogenates were decreased comparing to nontreated homogenates.
These results suggest that LDL-CE were mainly hydrolized at acid area in the microphage and arterial wall. And once hydrolized cholesterol oleate was resterified in the neutral area. Tocopherol may prevent the deposition of cholesterol ester by facilitating the hydrolysis of LDL-cholesterol ester in lysosome and by reducing the reesterification of once hydrolized cholesterol in microsome.
