Aluminum is a contaminant of commercial ATP. We have used the fluoresc
ent chelation agent morin to define the conditions of solution pH and
incubation period under which this contaminating aluminum was biologic
ally available. The biological significance of our model ligand morin
was tested in media in which the morin was replaced with the A beta P(
25-35) peptide. Aluminum-contaminated ATP was shown to promote the for
mation of Thioflavin T-reactive amyloid aggregates relative to equimol
ar concentrations of either aluminum added in the absence of ATP or al
uminum-free ATP. Our demonstration of the biological availability of a
luminum in commercial ATP should serve as a cautionary note to its use
in biochemistry, and might also be interpreted to invoke ATP as an in
tracellular (intraneuronal) pool of biologically available aluminum in
vivo.