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Myelin is a preferential target of aluminum-mediated oxidative damage.
Arch Biochem Biophys. 1997 Aug 15; 344(2):289-94.AB

Abstract

The capacity of Al3+ to promote oxidative damage to brain membranes was investigated both in vitro and in vivo. In vitro, Al3+ and related metals (Sc3+, Ga3+, In3+, Be2+, Y3+, and La3+) stimulated Fe2+-initiated lipid and protein oxidation in brain myelin and synaptic membranes. Al3+, Sc3+, Y3+, and La3+ significantly promoted protein-associated carbonyl production in myelin, while in synaptic membranes, the stimulatory effect was observed in the presence of Ga3+, In3+, Y3+, Sc3+, and La3+. In myelin the magnitude of the stimulation of lipid oxidation followed the order Sc3+, Y3+, La3+ > Al3+, Ga3+, In3+ > Be2+. When compared to mitochondria and microsomal and synaptic membranes, myelin showed a marked susceptibility to Al3+-mediated lipid peroxidation. The differential susceptibility of myelin compared to synaptic membranes could not be explained by differences in membrane composition, since the relative content of negatively charged phospholipids (binding sites) was similar for both membranes, and myelin had a lower content of poly-unsaturated fatty acids (substrates of lipid oxidation) and a higher concentration of alpha-tocopherol compared to synaptic membranes. In a model of Al3+ intoxication imposed to mice during pregnancy and early development, a 72% higher content of lipid peroxidation products was found in brain myelin. The fluidity of myelin evaluated by the polarization fluorescence of 1,3-diphenylhexatriene was significantly higher in the Al3+-intoxicated mice than in controls. Since myelin has a high relative content of lipid:protein compared to other membranes, these results support our hypothesis that ions without redox capacity can stimulate in vitro and in vivo lipid oxidation by promoting phase separation and membrane rigidification, thus accelerating lipid oxidation.

Authors+Show Affiliations

Department of Biological Chemistry, IQUIFIB (UBA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9264541

Citation

Verstraeten, S V., et al. "Myelin Is a Preferential Target of Aluminum-mediated Oxidative Damage." Archives of Biochemistry and Biophysics, vol. 344, no. 2, 1997, pp. 289-94.
Verstraeten SV, Golub MS, Keen CL, et al. Myelin is a preferential target of aluminum-mediated oxidative damage. Arch Biochem Biophys. 1997;344(2):289-94.
Verstraeten, S. V., Golub, M. S., Keen, C. L., & Oteiza, P. I. (1997). Myelin is a preferential target of aluminum-mediated oxidative damage. Archives of Biochemistry and Biophysics, 344(2), 289-94.
Verstraeten SV, et al. Myelin Is a Preferential Target of Aluminum-mediated Oxidative Damage. Arch Biochem Biophys. 1997 Aug 15;344(2):289-94. PubMed PMID: 9264541.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Myelin is a preferential target of aluminum-mediated oxidative damage. AU - Verstraeten,S V, AU - Golub,M S, AU - Keen,C L, AU - Oteiza,P I, PY - 1997/8/15/pubmed PY - 1997/8/15/medline PY - 1997/8/15/entrez SP - 289 EP - 94 JF - Archives of biochemistry and biophysics JO - Arch Biochem Biophys VL - 344 IS - 2 N2 - The capacity of Al3+ to promote oxidative damage to brain membranes was investigated both in vitro and in vivo. In vitro, Al3+ and related metals (Sc3+, Ga3+, In3+, Be2+, Y3+, and La3+) stimulated Fe2+-initiated lipid and protein oxidation in brain myelin and synaptic membranes. Al3+, Sc3+, Y3+, and La3+ significantly promoted protein-associated carbonyl production in myelin, while in synaptic membranes, the stimulatory effect was observed in the presence of Ga3+, In3+, Y3+, Sc3+, and La3+. In myelin the magnitude of the stimulation of lipid oxidation followed the order Sc3+, Y3+, La3+ > Al3+, Ga3+, In3+ > Be2+. When compared to mitochondria and microsomal and synaptic membranes, myelin showed a marked susceptibility to Al3+-mediated lipid peroxidation. The differential susceptibility of myelin compared to synaptic membranes could not be explained by differences in membrane composition, since the relative content of negatively charged phospholipids (binding sites) was similar for both membranes, and myelin had a lower content of poly-unsaturated fatty acids (substrates of lipid oxidation) and a higher concentration of alpha-tocopherol compared to synaptic membranes. In a model of Al3+ intoxication imposed to mice during pregnancy and early development, a 72% higher content of lipid peroxidation products was found in brain myelin. The fluidity of myelin evaluated by the polarization fluorescence of 1,3-diphenylhexatriene was significantly higher in the Al3+-intoxicated mice than in controls. Since myelin has a high relative content of lipid:protein compared to other membranes, these results support our hypothesis that ions without redox capacity can stimulate in vitro and in vivo lipid oxidation by promoting phase separation and membrane rigidification, thus accelerating lipid oxidation. SN - 0003-9861 UR - https://www.unboundmedicine.com/medline/citation/9264541/Myelin_is_a_preferential_target_of_aluminum_mediated_oxidative_damage_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0003-9861(97)90146-6 DB - PRIME DP - Unbound Medicine ER -