Coupling of Phosphorylation to Electron and Hydrogen Transfer by a Chemi-Osmotic type of Mechanism

Mitchell, Peter

doi:10.1038/191144a0

Cited by 4,165 publications

(2,067 citation statements)

References 17 publications

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“…Uncouplers abolish transmembrane potential by acting as protonophores [1]. As a result of the uncoupling, energy-linked functions, such as Ca 2÷ retention, become depressed [2].…”

Section: Introductionmentioning

confidence: 99%

“…As a result of the uncoupling, energy-linked functions, such as Ca 2÷ retention, become depressed [2]. The property of a molecule to act as uncoupler mainly depends on its pK and on its ability to be solubilized in the lipid milieu of the inner mitochondrial membrane [1]. Franklin and Cafiso [3] have shown that the incorporation of 6-ketocholestanol (kCh) to vesicles, formed by phosphatidyl choline, produces an increase in the binding and transport of hydrophobic ions by increasing the membrane dipole potential.…”

Section: Introductionmentioning

confidence: 99%

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On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

et al. 1996

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This work shows that 6-ketocholestanol (kCh) inhibits the effect of carbonyl cyanide-m-chlorophenyl hydrazone (CCP) on mitochondrial Ca 2÷ efflux. Such an effect proved to be caused by diminution of membrane fluidity, therefore, it is affected by the incubation temperature. Furthermore, kCh reversed CCPinduced Ca 2+ efflux depending on the accumulation of phosphate. It is also shown that kCh enhances the effect of carboxyatractyloside on membrane permeability transition.

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“…Uncouplers abolish transmembrane potential by acting as protonophores [1]. As a result of the uncoupling, energy-linked functions, such as Ca 2÷ retention, become depressed [2].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

et al. 1996

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“…The role of the H 1 as the coupling ion was proposed in 1961 by Peter Mitchell in his chemiosmotic theory (8). It was postulated that light and respiration energy are transduced into a Dl H þ , which is then used for ATP synthesis, solute transport, and motility (Fig.…”

Section: *These Authors Equally Contributed To This Articlementioning

confidence: 99%

The role of proton and sodium ions in energy transduction by respiratory complex I

2012

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SummaryRespiratory complex I plays a central role in energy transduction. It catalyzes the oxidation of NADH and the reduction of quinone, coupled to cation translocation across the membrane, thereby establishing an electrochemical potential. For more than half a century, data on complex I has been gathered, including recently determined crystal structures, yet complex I is the least understood complex of the respiratory chain. The mechanisms of quinone reduction, charge translocation and their coupling are still unknown. The H 1 is accepted to be the coupling ion of the system; however, Na 1 has also been suggested to perform such a role. In this article, we address the relation of those two ions with complex I and refer ion pump and Na 1 /H 1 antiporter as possible transport mechanisms of the system. We put forward a hypothesis to explain some apparently contradictory data on the nature of the coupling ion, and we revisit the role of H 1 and Na 1 cycles in the overall bioenergetics of the cell. IUBMBIUBMB Life, 64(6): 492-498, 2012

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“…Mitchell's success in using the proton-motive force to explain energy conversion in mitochondria (Mitchell, 1961) led to a considerable effort over the next three decades to explore the usefulness of nonequilibrium thermodynamics in biology (Caplan and Essig, 1983;Westerhoff and van Dam, 1987;Walz, 1990). Even if substantial progress was made, it was eventually concluded that the theory had major drawbacks.…”

Section: Introductionmentioning

confidence: 99%

Active transport: a kinetic description based on thermodynamic grounds

Kjelstrup

Rubı́

Bedeaux

2005

Journal of Theoretical Biology

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We show that active transport processes in biological systems can be understood through a local equilibrium description formulated at the mesoscale, the scale to describe stochastic processes. This new approach uses the method established by nonequilibrium thermodynamics to account for the irreversible processes occurring at this scale and provides nonlinear kinetic equations for the rates in terms of the driving forces.The results show that the application domain of nonequilibrium thermodynamics method to biological systems goes beyond the linear domain. A model for transport of Ca 2+ by the Ca 2+ -ATPase, coupled to the hydrolysis of adenosine-triphosphate is analyzed in detail showing that it depends on the reaction Gibbs energy in a non-linear way. Our results unify thermodynamic and kinetic descriptions, thereby opening new perspectives in the study of different transport phenomena in biological systems.

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Coupling of Phosphorylation to Electron and Hydrogen Transfer by a Chemi-Osmotic type of Mechanism

Cited by 4,165 publications

References 17 publications

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

The role of proton and sodium ions in energy transduction by respiratory complex I

Active transport: a kinetic description based on thermodynamic grounds

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Coupling of Phosphorylation to Electron and Hydrogen Transfer by a Chemi-Osmotic type of Mechanism

Cited by 4,165 publications

References 17 publications

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca2+ efflux

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca2+ efflux

The role of proton and sodium ions in energy transduction by respiratory complex I

Active transport: a kinetic description based on thermodynamic grounds

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On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux