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|Title:||Metal ion specificity in anaesthetic induced increase in the rate of monensin and nigericin mediated H+/ M+ exchange across phospholipid vesicular membranes|
|Authors:||Prabhananda, B S|
Kombrabail, Mamata H
|Abstract:||From a study or the decay or the pH difference across vesicular membranes (Δ pH) it has been possible to show that H+ and alkali metal ion (M+) concentration gradients across bilayer membranes (which are responsible for driving important biochemical processes) can be selectively perturbed by anaesthetics such as chloroform and benzyl alcohol by combining them with a suitable exchange ionophore. On adding the anaesthetic to the membrane in an environment containing metal ions M+=K+. the rate or Δ pH decay by H+/M+ exchange increases by a larger factor or by a smaller factor (when compared to that in a membrane environment with M+=Na+) depending on whether the exchange ionophore chosen is monensin or nigeriein. A rational explanation of this "metal ion specificity" can be given using the exchange ionophore mediated ion transport scheme in which the equilibrations at the "interfaces" are fast compared to the "translocation equilibration" between the species in the two layers of the membrane. The following three factors are responsible for the observed "specificity": On adding the anesthetic (i) translocation rate constants increase. (ii) the concentrations of the M+ bound ionophores increase at the expense of H+ bound ionophores. (iii) Under our experimental conditions the rate determining species are the complexes monensin-K (Mon-K) and nigeriein-H (Nig-H) for M+=K+ whereas they are monensin -H (MonH) and nigeriein-Na (Nig-Na) for M+=Na+ Possible anesthetic induced membrane perturbations contributing to the above mentioned changes in the membrane are (A), the loosening of the membrane structure and (B ), an associated increase in the membrane hydration (and membrane dielectric constant ). An analysis of the consequent changes in the various transport steps shows the following: (a), The anaesthetic induced changes in the translocation rates of electrically charged species are not relevant in the explanation or the observed changes in the Δ pH decay rates. (b), Changes in the rates of fast equilibria at the interface contribute to changes in KH and KM (c), A suggestion made in the literature, that a significant interaction between the dipole moment of the monensin-K complex and the membrane slows down its translocation, is not valid. (d), The ability to explain rationally all the Δ pH decay data confirms the validity or the transport scheme used. In our experiments Δ pH across the vesicular membrane was created by pH jump coming from a temperature jump.|
|ISSN:||0975-0959 (Online); 0301-1208 (Print)|
|Appears in Collections:||IJBB Vol.36(6) [December 1999]|
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