Electrostatic forces control the penetration of membranes by charged solutes

Intracellular turnover of Fluorescein diacetate. Influence of membrane ionic gradients on Fluorescein efflux

“…In model systems constituted by liposomes, it has been demonstrated that permeability of charged fluorescent compounds across the membrane is coupled to a concomitant permeation of counterions that restore electric balance (Bramhall, 1984). This evidence suggests that, in living ceils, Fluorescein permeability occuring after FDA turnover may be related to the ionic gradient (i.e.…”

“…The efflux of 5(6)~ carboxyfluorescein from lipid vesicles, for instance, has been shown to be dependent on the concomitant permeation rate of sodium ions (Bramhall, 1984). Given that Fluorescein is negatively-charged at physiological pH (Thomas, 1986), it seems reasonable to suppose that the release of this compound from living cells is also related to the transmembrane ionic gradient (i.e.…”

Permeability of Phospholipid Vesicles to the Tumor Antigen Epitope gp100280–288

“…This process produced mostly unilamellar and bilamellar vesicles, [23] the distribution of which was determined by steric exclusion chromatography as described below. To avoid the permeability changes associated with phase transition [16] and vesicle fusion, [24] from this point onward the vesicles were maintained below the lipid transition temperature.…”

“…[32,33] For class I-restricted epitopes the size and the relative importance of the charged terminals should imply relatively low permeability. [16,17] However, the generally low polarity of these peptides may imply an high partition coefficient with lipid, which may hamper the peptide release from the lipid. Therefore, as noted by Goren et al, [23] the role of this parameter is a priori unpredictable.…”

“…Among the factors controlling vesicle permeability, a relevant role is played by the size and polarity of the substance carried. [16,17] Permeability is also modified by cholesterol [18] and lipid-bound polymers. [19] Although formation of transient defects of the lipid layer [14] may control the diffusion of small charged species or the flux of species restricted by their interactions with the phospholipid aliphatic chains, [15,20] these mechanisms are unlikely to be meaningful in controlling vesicle permeability toward class I-restricted epitopes.…”