Oxygenated derivatives of cholesterol are believed to play a role in cellular cholesterol homeostasis through the feed-back control of its biosynthesis. We report that 26-hydroxycholesterol inhibits the specific binding, uptake and degradation of 125I-LDL in human fibroblasts. The effect is dose-dependent, and saturation kinetics indicates a reduction of LDL-binding sites with no effect on ligand affinity. The results support a possible role of 26-hydroxycholesterol, a physiological oxysterol, in the regulation of cellular cholesterol homeostasis.
