Aluminum, a metal without redox capacity in biological systems, potentiates
the stimulation of lipid peroxidation induced by Fe2+. In this study the i
nteractions between aluminum and oxidative stress induced by ascorbate (0.8
mM)/Fe2+ (2.5 mu M) in synaptosomes isolated from rat brain were investiga
ted The amount of Al3+ in aluminum solutions was calculated according to th
e Zatta protocol (Zatta er al., 1995), and lipid peroxidation was measured
by quantifying thiobarbituric acid-reactive substances (TBARS). In synaptos
omes under oxidizing conditions the addition of 11 mu M Al3+ increased the
formation of TEARS. In synaptosomes incubated in the absence of oxidants no
significant differences were found between the levels of lipid peroxidatio
n of synaptosomes incubated in the absence or in the presence of aluminum.
In the presence of an oxidizing system aluminum accumulation was significan
tly increased twofold in synaptosomes. Data suggest that the facilitation o
f aluminum accumulation during brain oxidative injury might contribute to a
luminum neurotoxicity and neuronal cell degeneration.