In reality, a number of processes act to dissipate the gradient, so electron transport never completely stops. Instead, the rate of electron transport is regulated by the rate at which the gradient is allowed to dissipate. The ability of the chemiosmotic gradient to limit electron transport is called respiratory control.
Of course, the primary purpose of mitochondria is to phosphorylate ADP. The energy needed to do that is stored as a gradient of protons. Presumably, if a proton were allowed to come back into the matrix there would be a release of energy. How can that energy be captured and exploited?
Embedded in the inner membrane among the structures of the electron transport system are structures called the ATP synthetase complex. The ATP synthetase complex consists of a proton channel and catalytic sites for the synthesis of ATP from ADP and phosphate. When ADP and phosphate are available, they bind the catalytic sites on the ATP synthetase. When this happens, the channel opens, and protons can come whooshing back in. The energy released is used to couple the phosphate to ADP, to make ATP.
The mechanism can be
likened to a water wheel, where the flow of protons resembles a flow of
water downhill, and the turning of the wheel is the turning of ADP toward
phosphate to cause the bond to form.
So...Energy from food is channeled by enzymes into the mitochondria, in which it is channeled to the ETS. The ETS uses the energy to produce a chemiosmotic gradient, which is maintained at a constant level by electron transport. Electron transport is limited by the presence of the gradient. By binding to ATP synthetase, ADP permits protons to enter the matrix through a special channel, using the released energy to create a covalent bond between ADP and phosphate. By providing an outlet for the protons, activation of ATP synthetase by ADP leaves room for more, allowing electron transport to proceed.
This has been an oversimplified overview, designed to organize your thoughts so you may proceed with the details presented in the main path. Nearly everything presented here must be modified to provide a true picture of how mitochondria function, both in vivo and experimentally.
Created by D.R. Caprette (firstname.lastname@example.org), Rice University, 1 May 1996
Updated 9 June 1997
above is from Rice University (click here for link to their web site).
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Metabolic Transformations - Why you can get fat by eating sugar (page 142)
|Outer membrane||Fat metabolism (energy), transport|
|Intermembrane space||Proton reservoir
|Inner membrane||Electron transport
Chemiosmosis - the importance of proton
gradient in driving transporters and in formation of ATP
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Last modified on: 31 January, 2000 by Dave Ussery