FLUORIDE EFFECTS ON CHOLESTEROL INFLUX AND EXPRESSION OF THE SCAVENGER RECEPTOR CD36 IN THP1 DIFFERENTIATED MONOCYTE/MACROPHAGE CELLS

As is now well known, chronic exposure to fluoride (F) can enhance inflammatory reactions that promote oxidative stress and the formation and production of reactive oxygen species (ROS). Increased levels of ROS cause oxidative modification of low-density lipoproteins (LDLs) and formation of atherogenic oxidized LDLs (ox-LDLs), which are internalized by the monocyte-derived macrophages via scavenger receptor CD36 involved in foam cells and atherosclerotic plaque formation. In this work, in the absence of studies on the influence of F on the expression of scavenger receptor CD36 and the subsequent influx of cholesterol into macrophages and their participation in inflammatory atherosclerotic development, we used adherent macrophages from human monocytic leukemia cells (THP-1) that were incubated for 48hr with 1, 3, 6, and 10 mu M NaF. We then measured CD36 expression, total cholesterol accumulation in the cells, and estimated oxidative stress intensity. Dosage-dependent effects of F were measured by changes in 8-isoprostane (8-iso PGF(2 alpha)), and scavenger receptor CD36 expression preceding cholesterol influx into the macrophages. Images from light microscopy showed an increased number of lipid droplets within the cells. The effect of F on macrophages thus appears to be connected with the ability of these cells to take up and accumulate F, which may then trigger or stimulate processes leading to the conversion of macrophages into foam cells that form atherosclerotic plaque.