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Metal ion specificity in anaesthetic induced increase in the rate of monensin and nigericin mediated H<sup>+</sup>/ M<sup>+</sup> exchange across phospholipid vesicular membranes

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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
 
Creator Prabhananda, B S
Kombrabail, Mamata H
 
Description 415-421
From a study or the decay or the pH difference across vesicular membranes
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.

 


 
Date 2012-12-31T20:08:56Z
2012-12-31T20:08:56Z
1999-12
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/15476
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.36(6) [December 1999]