Lipid peroxidation facilitates aluminum accumulation in rat brain synaptosomes.
Aluminum, a metal without redox capacity in biological systems, potentiates the stimulation of lipid peroxidation induced by Fe2+. In this study the interactions between aluminum and oxidative stress induced by ascorbate (0.8 mM)/Fe2+ (2.5 microM) in synaptosomes isolated from rat brain were investigated. The amount of Al3+ in aluminum solutions was calculated according to the Zatta protocol (Zatta et al., 1995), and lipid peroxidation was measured by quantifying thiobarbituric acid-reactive substances (TBARS). In synaptosomes under oxidizing conditions the addition of 11 microM Al3+ increased the formation of TBARS. In synaptosomes incubated in the absence of oxidants no significant differences were found between the levels of lipid peroxidation of synaptosomes incubated in the absence or in the presence of aluminum. In the presence of an oxidizing system aluminum accumulation was significantly increased twofold in synaptosomes. Data suggest that the facilitation of aluminum accumulation during brain oxidative injury might contribute to aluminum neurotoxicity and neuronal cell degeneration.
Amador
F C
FC
Center for Neurosciences of Coimbra, Department of Zoology, University of Coimbra, Portugal.
Santos
M S
MS
Oliveira
C R
CR
D000535:Aluminum / Q000009:adverse effects / Q000493:pharmacokinetics*; D000818:Animals; D001682:Biological Availability; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D013574:Synaptosomes / Q000737:chemistry*; D014018:Tissue Distribution
D000535:Aluminum