The Ionic Liquid Anion bis(fluorosulfonyl)imide is Membrane Permeable and Modifies Membrane Dipole Potential
Sprache des Vortragstitels:
8th ÖGMBT Annual Meeting 2016 - Life Sciences for the Next Generation
Sprache des Tagungstitel:
Christof Hannesschläger1, Kai Bittermann2, Kai-Uwe Goss2, Peter Pohl1
1Johannes Kepler University Linz, Institute of Biophysics, Gruberstr. 40, 4020 Linz, Austria
2Helmholtz Centre for Environmental Research, Permoserstr. 15, D-04318 Leipzig, Germany
Environmental bis(fluorosulfonyl)imide (FSI-) pollution may represent a health hazard since its high hydrophobicity suggests that it may be easily taken up via passive membrane diffusion. We tested the hypothesis using artificial planar lipid bilayers. Symmetrical titration of phosphatidyl-choline membranes with potassium-FSI resulted in electrical conductivity with non-linear I-V-characteristics indicating that the substance adsorbs to the interface. Membrane conductivity increases with anion concentrations up to 1 mM and declines at higher concentrations. To explain the non-monotonic behavior, we tested whether an increased membrane viscosity may be responsible. Stopped-Flow experiments ruled out the hypothesis as they revealed an altered water permeability of vesicular membranes. Likewise, we excluded an anion repelling effect of the membrane surface potential as Zeta-Potential measurements showed a modest decrease of surface potential of only -30 mV for 10 mM FSI-. However, the alignment of adsorbed FSI- in a direction opposite to the lipid dipoles resulted in a huge drop in membrane dipole potential as observed by measurements of the second harmonics of the capacitive current. This finding is in line with a FSI- induced drop in the permeability of other hydrophobic anions (the protonophore CCCP). We conclude that starting form 100 µM, the permeable FSI- facilitates the movement of positive charges across the membrane thereby altering the gating characteristics of voltage-dependent membrane channels, i.e. FSI- is affecting signal propagation in excitatory tissues.