A model of oxidative phosphorylation in mammalian skeletal muscle

Korzeniewski, Bernard; Zoladz, Jerzy A.

doi:10.1016/s0301-4622(01)00184-3

Cited by 166 publications

(191 citation statements)

References 52 publications

Supporting

Mentioning

184

Contrasting

Order By: Relevance

“…A K m value of 0.7 μM is also in agreement with the "apparent" K m value of 0.8 μM estimated by Korzeniewski and Zoladz 49 for the cytochrome-c oxidase reaction.…”

Section: Michaelis-menten Kinetics For Oxygen Consumptionsupporting

confidence: 90%

“…While RQ can vary from 0.7 (fat metabolism) to 1.0 (carbohydrate metabolism), a model for a regulated change in CO 2 production would require the model to include the major metabolic pathways (glycolysis, glycogenolysis, and TCA cycle) and oxidative phosphorylation 15,49 along with the present model to complete the link between O 2 consumption and CO 2 and H + production in the parenchymal cells.…”

Section: Assessment Of the Model's Featuresmentioning

confidence: 99%

See 1 more Smart Citation

Simultaneous Blood–Tissue Exchange of Oxygen, Carbon Dioxide, Bicarbonate, and Hydrogen Ion

Dash

Bassingthwaighte

2006

Ann Biomed Eng

View full text Add to dashboard Cite

A detailed nonlinear four-region (red blood cell, plasma, interstitial fluid, and parenchymal cell) axially distributed convection-diffusion-permeation-reaction-binding computational model is developed to study the simultaneous transport and exchange of oxygen (O 2 ) and carbon dioxide (CO 2 ) in the blood-tissue exchange system of the heart. Since the pH variation in blood and tissue influences the transport and exchange of O 2 and CO 2 (Bohr and Haldane effects), and since most CO 2 is transported as (bicarbonate) via the CO 2 hydration (buffering) reaction, the transport and exchange of and H + are also simulated along with that of O 2 and CO 2 . Furthermore, the model accounts for the competitive nonlinear binding of O 2 and CO 2 with the hemoglobin inside the red blood cells (nonlinear O 2 -CO 2 interactions, Bohr and Haldane effects), and myoglobin-facilitated transport of O 2 inside the parenchymal cells. The consumption of O 2 through cytochrome-c oxidase reaction inside the parenchymal cells is based on MichaelisMenten kinetics. The corresponding production of CO 2 is determined by respiratory quotient (RQ), depending on the relative consumption of carbohydrate, protein, and fat. The model gives a physiologically realistic description of O 2 transport and metabolism in the microcirculation of the heart. Furthermore, because model solutions for tracer transients and steady states can be computed highly efficiently, this model may be the preferred vehicle for routine data analysis where repetitive solutions and parameter optimization are required, as is the case in PET imaging for estimating myocardial O 2 consumption.

show abstract

“…A K m value of 0.7 μM is also in agreement with the "apparent" K m value of 0.8 μM estimated by Korzeniewski and Zoladz 49 for the cytochrome-c oxidase reaction.…”

Section: Michaelis-menten Kinetics For Oxygen Consumptionsupporting

confidence: 90%

Section: Assessment Of the Model's Featuresmentioning

confidence: 99%

Simultaneous Blood–Tissue Exchange of Oxygen, Carbon Dioxide, Bicarbonate, and Hydrogen Ion

Dash

Bassingthwaighte

2006

Ann Biomed Eng

View full text Add to dashboard Cite

show abstract

“…While, as for complexes I and III, the flux is formulated to drive the system toward thermodynamic equilibrium, additional multiplicative factors have been included in order to successfully reproduce the observed data. The factor 1=ð1 þ k O2 =½O 2 Þ is included in equation 9 to account for the observed dependence of the rates of oxygen consumption and ATP generation on oxygen concentration [6,[19][20][21]26,27]. It will be shown that the factor [cytC(red) 2þ ]/ cytC tot is found to provide better fits to the observed data than are possible without it.…”

Section: Synopsismentioning

confidence: 99%

“…ANT flux involves the displacement of one negative charge from the matrix to the IM space, and is therefore coupled to the electrostatic membrane potential. The following empirical expression [4,6] is used to model the ANT flux:…”

Section: Synopsismentioning

confidence: 99%

“…For example, the widely used model of Korzeniewski and Zoladz [4][5][6] invokes an empirical linear relationship between the difference in pH across the mitochondrial inner membrane (matrix pH minus cytosol pH) and the magnitude of inner membrane potential. While the Korzeniewski model has been validated and verified based on a number of studies and is widely applied [7][8][9], the central empirical relationship between electrostatic potential and pH difference is not expected to apply under all conditions.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A Biophysical Model of the Mitochondrial Respiratory System and Oxidative Phosphorylation

Beard¹

2005

PLoS Comp Biol

106

View full text Add to dashboard Cite

A computational model for the mitochondrial respiratory chain that appropriately balances mass, charge, and free energy transduction is introduced and analyzed based on a previously published set of data measured on isolated cardiac mitochondria. The basic components included in the model are the reactions at complexes I, III, and IV of the electron transport system, ATP synthesis at F 1 F 0 ATPase, substrate transporters including adenine nucleotide translocase and the phosphate-hydrogen co-transporter, and cation fluxes across the inner membrane including fluxes through the K þ /H þ antiporter and passive H þ and K þ permeation. Estimation of 16 adjustable parameter values is based on fitting model simulations to nine independent data curves. The identified model is further validated by comparison to additional datasets measured from mitochondria isolated from rat heart and liver and observed at low oxygen concentration. To obtain reasonable fits to the available data, it is necessary to incorporate inorganic-phosphatedependent activation of the dehydrogenase activity and the electron transport system. Specifically, it is shown that a model incorporating phosphate-dependent activation of complex III is able to reasonably reproduce the observed data. The resulting validated and verified model provides a foundation for building larger and more complex systems models and investigating complex physiological and pathophysiological interactions in cardiac energetics.

show abstract

Integrated and Organized Cellular Energetic Systems

Saks

Monge

Guzun

et al. 2009

Wiley Encyclopedia of Chemical Biology

View full text Add to dashboard Cite

Bioenergetics as a part of biophysical chemistry and biophysics is a quantitative science that is based on several fundamental theories. The definition of energy itself is given by the first law of thermodynamics, and application of the second law of thermodynamics shows that the living cells can only function as open systems in which internal order (low entropy state) is maintained by increasing the entropy in surrounding medium (Schrödinger's principle of negentropy). For this mechanism, exchange of mass is needed that yields metabolism as the sum of catabolism and anabolism. The free‐energy changes taking place during metabolic reactions obey rules of chemical thermodynamics, which deals with Gibbs free energy of chemical reactions and with electrochemical potentials. For application of these theories to the integrated systems in vivo , complex cellular organization should be accounted for: macromolecular crowding, metabolic channeling and functional coupling mechanisms caused by close and tight protein–protein interactions, compartmentation of enzymes, as well as both macrocompartmentation and microcompartmentation of substrates and metabolites in cells should be considered. For integration of these system components, effective methods of communication, including compartmentalized energy transfer systems, are required. These systems are represented in muscle cells by phosphotransfer networks, mostly by creatine kinase and adenylate kinase systems. System analysis of these networks shows their central role both in energy transfer and metabolic feedback regulation of mitochondrial function, in regulation of ion fluxes and cellular energetics during increased workload by synchronizing the cellular electrical and mechanical activities with energy supply and substrate oxidation.

show abstract

A model of oxidative phosphorylation in mammalian skeletal muscle

Cited by 166 publications

References 52 publications

Simultaneous Blood–Tissue Exchange of Oxygen, Carbon Dioxide, Bicarbonate, and Hydrogen Ion

Simultaneous Blood–Tissue Exchange of Oxygen, Carbon Dioxide, Bicarbonate, and Hydrogen Ion

A Biophysical Model of the Mitochondrial Respiratory System and Oxidative Phosphorylation

Integrated and Organized Cellular Energetic Systems

Contact Info

Product

Resources

About