RESUMO
OBJECTIVE: Al(3+) stimulates Fe(2+) induced lipid oxidation in liposomal and cellular systems. Low-density lipoprotein (LDL) oxidation may render the particle atherogenic. As elevated levels of Al(3+) and increased lipid oxidation of LDL are found in sera of hemodialysis patients, we investigated the influence of Al(3+) on LDL oxidation. MATERIALS AND METHODS: Using different LDL modifying systems (Fe(2+), Cu(2+), free radical generating compounds, human endothelial cells, hemin/H(2)O(2) and HOCl), the influence of Al(3+) on LDL lipid and apoprotein alteration was investigated by altered electrophoretic mobility, lipid hydroperoxide-, conjugated diene- and TBARS formation. RESULTS: Al(3+) could stimulate the oxidizability of LDL by Fe(2+), but not in the other systems tested. Al(3+) and Fe(2+) were found to bind to LDL and Al(3+)could compete with Fe(2+) binding to the lipoprotein. Fluorescence polarization data indicated that Al(3+) does not affect the phospholipid compartment of LDL. CONCLUSIONS: The results indicate that increased LDL oxidation by Fe(2+) in presence of Al(3+) might be due to blockage of Fe(2+) binding sites on LDL making more free Fe(2+) available for lipid oxidation.
