Physical partitioning is the main mechanism of alpha-tocopherol and cholesterol transfer between lipoproteins and P388D1 macrophage-like cells
Abstract
The regulation of cellular vitamin E concentration was studied in P388D1 macrophage-like cells. Cellular alpha-tocopherol levels increased more than 5000-fold over constitutive levels without reaching saturation when P388D1 cells were cultured in vitamin-E-supplemented fetal calf serum. The uptake of alpha-tocopherol was accompanied by accumulation of alpha-[3H]tocopherol and [14C]cholesterol in these cells. Human unmodified low-density lipoprotein (LDL) inhibited the uptake of alpha-[3H]tocopherol and [14C]cholesterol in a dose-dependent manner and with very similar IC50. Acetylated, Cu2+-oxidized and aggregated human LDL and human very-low-density-lipoprotein (VLDL) were similarly potent, whereas human HDL was at least tenfold less effective than human LDL when inhibitory activity was correlated to lipoprotein protein levels. The rate of vitamin E uptake by P388D1 cells, however, always correlated with the extracellular alpha-tocopherol/cholesterol ratio. Efflux of alpha-[3H]tocopherol from labeled P388D1 cells required extracellular acceptors and was accompanied by the concomitant release of [14C]cholesterol. Both human LDL and HDL could serve as acceptors. Changes in the cellular alpha-tocopherol level appear to be the dire...Continue Reading
References
Endothelial and smooth muscle cells alter low density lipoprotein in vitro by free radical oxidation
Inhibition of protein kinase C activity and vascular smooth muscle cell growth by d-alpha-tocopherol
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