TY - JOUR
T1 - Aluminum Has Both Oxidant and Antioxidant Effects in Mouse Brain Membranes
AU - Oteiza, Patricia I
AU - Fraga, C. G.
AU - Keen, C. L.
PY - 1993/1
Y1 - 1993/1
N2 - The in vitro effects of aluminum (A1) on lipid peroxidation were studied in mouse brain homogenates and purified brain subcellular fractions. In brain homogenates prepared in 5 mM Na2HPO4, 0.14 M NaCl, pH 7.4, the addition of Al decreased Fe2+-induced lipid peroxidation, measured as 2-thiobarbituric acid- reactive substances (TBARS), in a dose dependent manner, with a maximum effect at 250 μM Al. In brain homogenates prepared in 20 mM Tris-HCI, 0.14 M NaCl, pH 7.4, Al acted as a prooxidant at 250 and 500 μM concentrations. The prooxidant effect of Al was enhanced with increasing concentrations of Fe2+. In brain microsonies Al increased TBARS production and conjugated dienes formation, both depending on the addition of Fe2+. In myelin, the prooxidant effect of Al on Fe2+-induced lipid peroxidation was eliminated when membranes were disrupted with 0.2% Triton X-100. Thus, in brain homogenates, microsomes, and myelin, Al has the potential for exhibiting both prooxidant and antioxidant activity depending on the concentration of Fe2+ and Al in the media and on membrane integrity. Similar to Al, Be2+ and La3+ had prooxidant effects on Fe2+-induced lipid peroxidation in myelin, suggesting that membrane damage secondary to induced lipid peroxidation may be a common mechanism underlying tissue pathology even with metals without redox capacity. Oxidative damage to brain cell components may be an important mechanism mediating the neurotoxicity of Al.
AB - The in vitro effects of aluminum (A1) on lipid peroxidation were studied in mouse brain homogenates and purified brain subcellular fractions. In brain homogenates prepared in 5 mM Na2HPO4, 0.14 M NaCl, pH 7.4, the addition of Al decreased Fe2+-induced lipid peroxidation, measured as 2-thiobarbituric acid- reactive substances (TBARS), in a dose dependent manner, with a maximum effect at 250 μM Al. In brain homogenates prepared in 20 mM Tris-HCI, 0.14 M NaCl, pH 7.4, Al acted as a prooxidant at 250 and 500 μM concentrations. The prooxidant effect of Al was enhanced with increasing concentrations of Fe2+. In brain microsonies Al increased TBARS production and conjugated dienes formation, both depending on the addition of Fe2+. In myelin, the prooxidant effect of Al on Fe2+-induced lipid peroxidation was eliminated when membranes were disrupted with 0.2% Triton X-100. Thus, in brain homogenates, microsomes, and myelin, Al has the potential for exhibiting both prooxidant and antioxidant activity depending on the concentration of Fe2+ and Al in the media and on membrane integrity. Similar to Al, Be2+ and La3+ had prooxidant effects on Fe2+-induced lipid peroxidation in myelin, suggesting that membrane damage secondary to induced lipid peroxidation may be a common mechanism underlying tissue pathology even with metals without redox capacity. Oxidative damage to brain cell components may be an important mechanism mediating the neurotoxicity of Al.
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U2 - 10.1006/abbi.1993.1070
DO - 10.1006/abbi.1993.1070
M3 - Article
C2 - 8424688
AN - SCOPUS:0027301756
VL - 300
SP - 517
EP - 521
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 1
ER -