Alcohols produce reversible and irreversible acceleration of phospholipid flip-flop in the human erythrocyte membrane

Schwichtenhövel, C; Deuticke, B; Haest, CW

HERO ID

4674891

Reference Type

Journal Article

Year

1992

Language

English

PMID

1390862

HERO ID 4674891
In Press No
Year 1992
Title Alcohols produce reversible and irreversible acceleration of phospholipid flip-flop in the human erythrocyte membrane
Authors Schwichtenhövel, C; Deuticke, B; Haest, CW
Journal Biochimica et Biophysica Acta
Volume 1111
Issue 1
Page Numbers 35-44
Abstract The slow, non-mediated transmembrane movement of the lipid probes lysophosphatidylcholine, NBD-phosphatidylcholine and NBD-phosphatidylserine in human erythrocytes becomes highly enhanced in the presence of 1-alkanols (C2-C8) and 1,2-alkane diols (C4-C8). Above a threshold concentration characteristic for each alcohol, flip rates increase exponentially with the alcohol concentration. The equieffective concentrations of the alcohols decrease about 3-fold per methylene added. All 1-alkanols studied are equieffective at comparable calculated membrane concentrations. This is also observed or the 1,2-alkane diols, albeit at a 5-fold lower membrane concentration. At low alcohol concentrations, flip enhancement is reversible to a major extent upon removal of the alcohol. In contrast, a residual irreversible flip acceleration is observed following removal of the alcohol after a treatment at higher concentrations. The threshold concentrations to produce irreversible flip acceleration by 1-alkanols and 1,2-alkane diols are 1.5- and 3-fold higher than those for flip acceleration in the presence of the corresponding alcohols. A causal role in reversible flip-acceleration of a global increase of membrane fluidity or membrane polarity seems to be unlikely. Alcohols may act by increasing the probability of formation of transient structural defects in the hydrophobic barrier that already occur in the native membrane. Membrane defects responsible for irreversible flip-acceleration may result from alterations of membrane skeletal proteins by alcohols.
Doi 10.1016/0005-2736(92)90271-M
Pmid 1390862
Wosid WOS:A1992JV02600005
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English