HELP! Interesting molecular transport argument...

Jason Comander jcomand at
Tue Oct 25 01:19:00 EST 1994

	A friend and I are having a huge disagreement over a
fundamental concept in biochemistry and enzymology- Can a cell do
anything to speed up an oxygen molecule's transit from the cell
membrane to a mitochondria in the middle of the cell?  I would
appreciate any of your input to help us work this out.
	He was asked to hypothetically redesign the human body to
operate under lower atmospheric oxygen.  He proposed that the cell
be redesigned to have an "oxygen ferry" to speed up oxygen's
transit to the mitochondria by reducing the distance that the
oxygen molecule has to sluggishly diffuse through.  It could use
a ferry, which would transport it faster.  The ferry would be bound
to the cell membrane until an oxygen molecule floated into the
cell.  The oxygen molecule would bind to the ferry, and the ferry
would be released from the cell membrane to move toward the
mitochondria.  There would be a ligand on the ferry that is
complementary to a receptor on the mitochondria.  Thus, the
ferry/oxygen complex would be drawn toward the mitochondria because
the ligand/receptor binding would be energetically favorable.  When
the ferry/oxygen complex arrived at the mitochondria, the oxygen
would be released.
	My friend contends that this process would lessen the time it
takes for the oxygen to get from the cell membrane to the
mitochondria.  Instead of the oxygen molecule randomly diffusing
around the cell, the ferry/oxygen complex would be drawn toward the
mitochondria.  The movement of oxygen from the cell membrane to the
mitochondria is energetically favorable, thus it will be faster. 
He points out that in the Ras pathway, Raf has a transport molecule
which localizes it near Ras so that a reaction between Ras and Raf
can occur.  Why would this system exist otherwise, if Raf could
just diffuse toward Ras?
	I say that in a system as big as a cell (a few microns), the
ferry/oxygen complex would not be able to "feel" the electrostatic
pull of the receptor on the mitochondria until it got "in the
neighborhood" of the mitochondria.  For the vast(?) majority of its
trip, the ferry/oxygen complex would be diffusing with no
particular reason to move in the direction of the mitochondria. 
Given that larger molecules diffuse more slowly, the ferry/oxygen
complex will diffuse to the mitochondria _slower_ than the free
oxygen molecule.
	Who's right?  Can a cell do anything to speed up an oxygen
molecule's transit from the cell membrane to a mitochondria in the
middle of the cell?

	Argument #2.  Getting frustrated with the above argument, we
managed to create another one about concentration gradients.  Let's
say that many copies of our hypothetical enzyme can store up a
large number of oxygen molecules near the mitochondria.  Assuming
our system is at equilibrium, there would be no oxygen
concentration gradient, because entropy will equalize the
concentration of oxygen to the same value everywhere.  The question
is:  When calculating the concentration of oxygen molecules in the
area around the mitochondria, do the bound oxygen molecules get
counted?  i.e. Can a free oxygen molecule entering the neighborhood
of the mitochondria "see" that there are really hundreds of (bound)
oxygen molecules all around it, and that it shouldn't be there
because the oxygen concentration is high? even though the bound
oxygens are hidden deep within an enzyme?
	I guess it would make sense to answer this question before
talking about the same situation _with_ concentration gradients.

	I hope you find these arguments as interesting as I do!

	Many thanks,
	Jason Comander

Jason Comander
Harvard University
(617) 493-3199

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