Role of the lipid bilayer at the dielectric relaxations in human erythrocytes

Abstract

AbstractUsing the dielectric changes in red blood cells (RBCs) at the temperature of spectrin dissociation and denaturation,TA, two dielectric relaxations have been detected on spectrin network, βsprelaxation at 1.4 MHz and γ1sprelaxation at 9 MHz. In this study, the βsprelaxation was linearly strengthened on increasing the ion accumulation at either side of RBC plasma membranes, while the strength of γ1sprelaxation remained unaffected. In Triton shells, produced by mild extraction of RBC ghost membrane lipids by Triton-X-100 (up to 0.1%) and in RBCs, treated by acid medium (pH 5.2), known to disconnect the glycophorin C integral protein from the actin-spectrin junction, the βsprelaxation was strongly to fully inhibited while γ1sprelaxation was preserved. In RBCs, acid-treated RBCs, RBC ghost membranes and Triton-X shells the capacitance contribution and dielectric loss curve of spectrin network were both positive for βsprelaxation and negative for γ1sprelaxation. The above results support the view that βsprelaxation exhibits piezo effect on spectrin network prior toTA, powered by the electrodeformation of lipid membrane mainly through the glycophorin C-actin-spectrin bridge. This piezo effect adds strength (~ 25%) to the interfacial polarization of RBC lipid membrane and could be adjuvant factor in the elasticity and flicker of RBC membrane. The results and the amended equivalent circuit of RBC suspension support the claim that γ1sprelaxation reflects direct interaction and resonance of the field with the natural oscillations of dipoles (segments) of spectrin tetramers.