PATHWAYS OF VIOLOGEN-MEDIATED OXIDATION REDUCTION REACTIONS ACROSS DIHEXADECYL PHOSPHATE BILAYER-MEMBRANES

Transmembrane reduction of methylviologen (N,N-dimethyl-4,4'-bipyridinium, MV2+) and several n-alkylmethyl analogs, i.e., N-alkyl-N'-methyl-4,4'-bipyridinium (C(n)MV2+, n less-than-or-equal-to 10), entrapped within dihexadecyl phosphate (DHP) vesicles by S2O42- or CrEDTA2- located in the bulk aqueous phase occurred only when viologens were also initially present on the same side of the membrane as the reductant. Viologen radical cation formation was biphasic, with reduction of the externally bound viologen dications preceding reduction of the entrapped viologen. For MV2+, the rate law was d[MV+]/dt = k(a)[MV2+]o[SO2-]o + k(b)[MV+]o[MV2+]i, where the subscripts i and o refer to viologens bound at the vesicle inner and outer interfaces, respectively. Transmembrane reduction was accompanied by comigration of a viologen radical cation with each electron transferred across the bilayer. The MV+ ion formed on the external surface was monomeric, but the MV+ formed internally was aggregated (or multimeric); from the wavelength dependence of the kinetic curves, it was shown that aggregation coincided with or rapidly followed the rate-limiting transmembrane redox step. For the C(n)MV2+ ions, the reaction dynamics were qualitatively similar but were complicated by the simultaneous presence of both monomeric and multimeric forms of C(n)MV+ at the outer vesicle interface. When n > 10, reduction of external C(n)MV2+ ions was biphasic. For C16MV2+, only about one-third of the entrapped viologen was reducible unless the reaction medium also contained lipophilic ions, under which conditions all of the internal ions could be reduced. Correspondingly, only one-third of the external C16MV2+ translocated to the inner vesicle surface. Computer simulations of the complex kinetic waveforms required inclusion of two independent transmembrane redox steps to obtain adequate data fits. There were interpreted in terms of two distinct reaction pathways involving (i) transverse diffusion of interfacially bound reactants and (ii) electron tunneling between the viologen radical cations and dications juxtaposed in the opposite bilayer leaflets. Possible alternative molecular mechanisms corresponding to the two pathways are discussed.