Oral administration of
lanthanum chloride (LaCl(3)) was reported to inhibit
atherosclerosis in experimental animals, but the mechanism was not clear. In the present work, the effects of La(III) and other
lanthanide ions (Ln(III)) on Cu(II)-induced oxidation of isolated
low-density lipoprotein (
LDL) and the related mechanism were investigated. By monitoring the formation of conjugated dienes (CD), low concentrations of La(III), Gd(III) and Y(III) were found to inhibit Cu(II)-induced
LDL oxidation kinetically, as characterized by the prolongation of the lag time, the decrease of the maximal accumulation of CD, and the maximal rate of CD accumulation. Using
5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and
alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) as spin trapping agents, the electron spin resonance (ESR) results showed that La(III) and Gd(III) at low concentrations significantly decreased the level of
free radicals, including
alkoxyl radical (LO*), alkyl radical (L*), and a transient radical, alkylperoxyl radical (LOO*), generated during
LDL oxidation induced by Cu(II). In addition, Fourier-transform infrared spectroscopy (FT-IR) study revealed that La(III) might cause the conformational change and the less aggregation of
apolipoprotein B-100 (
apoB) in
LDL, as demonstrated by the decreasing contents of alpha-helix, intermolecular beta-sheet, unordered structure and beta-turns, and the increasing contents of intramolecular beta-sheet and beta-strands. The inhibitory effect of Ln(III) on Cu(II)-induced
LDL oxidation was discussed on the basis of the decreased
free radical level and the second structural changes of
apoB in
LDL.