Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 375, Issue 2, Pages 340-346Publisher
ACADEMIC PRESS INC
DOI: 10.1006/abbi.1999.1671
Keywords
aluminum; Lipid domains; phase state; membrane dehydration; lipid oxidation
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The aim of the present study was to further understand how changes in membrane organization can lead to higher rates of lipid oxidation. We previously demonstrated that Al3+, SC3+, (Ga3+) Be2+, Y3+, and La3+ promote lipid packing and lateral phase separation. Using the probe Laurdan, we evaluated in liposomes if the higher rigidity of the membrane caused by Al3+ can alter membrane phase state and/or hydration, and the relation of this effect to Al3+-stimulated lipid oxidation. In liposomes of dimyristoyl phosphatidylcholine and dimyristoyl phosphatidylserine, Al3+ (10-100 mu M) induced phase coexistence and displacement of T-m. In contrast, in liposomes of brain phosphatidylcholine and brain phosphatidylserine, Al3+ (10-200 mu M) did not affect membrane phase state but increased Laurdan generalized polarization (GP = -0.04 and 0.09 in the absence and presence of 200 mu M Al3+, respectively). Sc3+, Ga3+, Be2+, Y3+, and La3+ also increased GP values, with an effect equivalent to a decrease in membrane temperature between 10 and 20 degrees C. GP values in the presence of the cations were significantly correlated (r(2) = 0.981 P < 0.001) With their capacity to stimulate Fe2+-initiated lipid oxidation. Metal-promoted membrane dehydration did not correlate with ability to enhance lipid oxidation, indicating that dehydration of the phospholipid polar headgroup is not a mechanism involved in cation-mediated enhancement of Fe2+-initiated lipid oxidation. Results indicate that changes in membrane phospholipid phase state favoring the displacement to gel state can facilitate the propagation of lipid oxidation. (C) 2000 Academic Press.
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