Aluminum facilitation of iron-mediated lipid peroxidation is dependent on substrate, pH and aluminum and iron concentrations.

It has been suggested that aluminum (Al) plays a role in neurological disorders. The mechanism of its neurotoxicity has not been established. Brain lipid peroxidation (LP) contributes to neurodegeneration. There have been conflicting reports concerning the Al effect on LP. In the present study, LP of three Folch Fractions from bovine brain and five pure phospholipids was determined in the presence of varying concentrations of iron (Fe) and Al at pH 5.5 and 7.4. Lipid peroxidation was measured as thiobarbituric acid reactive substances. Iron initiated LP, whereas Al did not. However, Al significantly facilitated Fe-mediated LP of bovine brain Folch Fractions I and III, bovine brain-derived phosphatidylserine, and egg yolk phosphatidylcholine. Bovine brain phosphatidylserine was the most susceptible substrate among the lipids tested. Aluminum facilitation of LP was Al and Fe concentration dependent. The peroxidation was greater at pH 5.5 than 7.4. There was no significant Al effect with Folch Fraction V, bovine brain-derived phosphatidylethanolamine, phosphatidylcholine, or sphingomyelin. This study confirmed the ability of Al to facilitate Fe-mediated LP and identified the substrates, pH, and Al concentrations favoring the peroxidation. A potential mechanism for Al facilitation of Fe-mediated LP is proposed.