UPTAKE OF RADIOLABELED AND COLLOIDAL GOLD-LABELED CHYLE CHYLOMICRONS AND CHYLOMICRON REMNANTS BY RAT PLATELETS IN-VITRO

This study examined the uptake of chyle chylomicrons (CMs) and chylomi cron remnants (CMRs) by rat platelets in vitro. CMs and CMRs were doub ly labeled with [H-3]arachidonate ([H-3]-20:4) and [C-14]cholesterol a nd were incubated with platelets for up to 4 hours. A significant upta ke (binding and/or internalization) of CMs by the platelets occurred, as indicated by the parallel increase of [H-3]20:4 and [C-14]cholester ol in platelets with incubation time. Addition of unlabeled CMs, VLDLs , LDLs, and HDLs decreased the uptake of labeled CMs. The competition experiments suggested that there is both a saturable binding and a non specific uptake of CMs. During incubation with CMs, the proportion of [H-3]20:4 in phospholipids decreased and that in 1,2-x-diacyl-glycerol increased. The data indicated that a phospholipase C-mediated degrada tion of phosphatidylcholine and phosphatidylethanolamine occurred, whe reas [H-3]20:4 in triglycer ide and C-14 in cholesteryl ester did not change. Electron microscopic studies after incubation with colloidal g old-labeled CMs (CM-Au's) demonstrated an accumulation of CM-Au partic les in the open canalicular system of the platelets. Some CM-Au partic les were localized in cytoplasmic vacuoles that were not stained by ru thenium red. Some CM-Au's or free gold particles were in vacuoles that showed acid phosphatase activity, indicating that some true endocytos is of CM occurred. The uptake of [H-3]-20:4- and [C-14]cholesterol-lab eled CMRs was low compared with the uptake of CMs. After incubation wi th colloidal gold-labeled CMRs (CMR-Au's), only a few platelets contai ned CMR-Au in their open canalicular systems, and no CMR-Au particles were seen in the cytoplasm or in acid phosphatase-positive vacuoles. R at platelets can thus interact with CMs by a process that leads to a s equestration in the open canalicular system and endocytosis and a net degradation of CM phospholipids. The conversion of CMs to CMRs counter acts this interaction.