Interactions of inorganic mercury with phospholipid micelles and model membranes. A P-31-NMR study

The binding of inorganic mercury Hg(II) to phospholipid headgroups has been investigated by phosphorus-31 nuclear magnetic resonance of phosphatidylethanolamine (PE), phosphatidylserine (PS and phosphatidylcholine (PC) in water micellar and multilamellar phases. HgCl2 triggers the aggregation of phospholipid micelles, leading to a lipid-mercury precipitate that is no longer detectable by high-resolution P-31-NMR. The remaining signal area corresponds to micelles in the soluble fraction and is a non-linear function of the initial mercury-to-lipid molar ratio. Kinetics of micelle aggregation are ex exponential for the first 15 min and show a plateau tendency after 120 min. Apparent Hg(II) affinities for phospholipid headgroups are in the order: PE > PS > PC. The same binding specificity is observed when HgCl2 is added to (1:1) mixtures of different micelles (PE + PC; PS + PC). However, mercury binding to mixed micelles prepared with two lipids (PE/PC or PS/PC) induces the aggregation of both lipids. Hg(II) also leads to a P-31-NMR chemical shift anisotropy decrease of PC, PS and mixed (1:1) PE/PC multilamellar vesicles and markedly broadens PS spectra. This indicates that HgCl2 binding forces phospholipid head-groups to reorient and that the concomitant network formation leads to a slowing down of PS membrane collective motions. Formation of a gel-like lamellar phase characterized by a broad NMR linewidth is also observed upon HgCl2 binding to PE samples both in fluid (L(alpha) or hexagonal (H-II) phases. The PE hexagonal phase is no longer detected in the presence of HgCl2. Mixed PE/PC dispersions remain in the fluid phase upon mercury addition, indicating that no phase separation occurs. Addition of excess NaCl leads to the appearance of the non-reactive species HgC42- and induces the reversal of all the above effects.