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Difference between revisions of "Gnaiger 2020 BEC MitoPathways"

From Bioblast
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|authors=Gnaiger E
|authors=Gnaiger E
|year=2012
|year=2012
|abstract=''In preparation''
|abstract=
 
 
 
|keywords=ETS, Q-junction, respiratory states, flux control ratios
|keywords=ETS, Q-junction, respiratory states, flux control ratios
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS
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|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
}}
}}
__TOC__
= Supplementary information =
* '''Preface'''
== Chapter 1. OXPHOS analysis ==
== Chapter 2. Mitochondrial pathways to Complex I: Respiratory substrate control with pyruvate, malate and glutamate ==
=== Notes - Pitfalls ===
2.1. Schwerzmann et al (1989) Proc Natl Acad Sci U S A 86: 1583-1587. “Of the substrates used here, pyruvate/malate activates the chain at complex I, glutamate/malate and succinate at complexes II and III, ..”
2.2. Ponsot et al (2005) J Cell Physiol 203: 479-486. (a) Respiration (State 3) in permeabilized fibres with malate alone gave 25-50% of the flux with pyruvate+malate. This most likely indicates a large content of endogenous mitochondrial substrates, which interfere to an unknown degree with the kinetics of respiration after addition of exogenous substrates. In such a study, the conventional initial depletion of endogenous substrates would be most important. (b) Maximal respiration rates in muscle should be evaluated at saturating or high Pi, since at a Pi concentration of 3 mM OXPHOS respiration is phosphate limited.
2.3. Hulbert et al (2006) J Comp Physiol B 176: 93-105. Addition of ‘sparking malate concentrations’. This term can probably be derived from the misconception that tricarboxylic acid cycle intermediates are conserved during respiration of isolated mitochondria. 380 µM malate (instead of mM concentrations) in conjunction with 2.4 mM pyruvate were used, which makes a comparison difficult between different tissues and different species: the low malate concentration may limit PMP flux at various degrees in the different sources of mitochondria, and GMP may support higher fluxes than PMP at tissue- and species-specific degrees.
=== References Chapter 2 ===
== Chapter 3. Mitochondrial pathways to Complex II. Glycerophosphate dehydrogenase and electrontransferring flavoprotein ==
== Chapter 4. Mitochondrial pathways to Complexes I+II:  Convergent electron transfer at the Q-Junction and additive effect of substrate combinations
== Chapter 5. Respiratory states, coupling control and coupling control ratios
== Chapter 6. Conversions of metabolic fluxes
== Apendix ==
=== A1. Respiratory coupling states and coupling control ratios ===
=== A2. Substrates, uncouplers and inhibitors ===

Revision as of 09:14, 25 November 2012

Publications in the MiPMap
Gnaiger E ed (2012) Mitochondrial Pathways and Respiratory Control. An Introduction to OXPHOS Analysis. Mitochondr Physiol Network 17.##: ## pp. 3rd ed. ISBN 978-3-9502399-6-6

» MiPNet2007

Gnaiger E (2012)

Abstract: Keywords: ETS, Q-junction, respiratory states, flux control ratios

O2k-Network Lab: AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS


Labels:


Organism: Human, Mouse  Tissue;cell: Skeletal muscle, Fibroblast  Preparation: Permeabilized cells, Permeabilized tissue, Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. 

Regulation: Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.  Coupling state: LEAK, ROUTINE, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Theory, MiPNet-Publication"MiPNet-Publication" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property. 


Supplementary information

  • Preface

Chapter 1. OXPHOS analysis

Chapter 2. Mitochondrial pathways to Complex I: Respiratory substrate control with pyruvate, malate and glutamate

Notes - Pitfalls

2.1. Schwerzmann et al (1989) Proc Natl Acad Sci U S A 86: 1583-1587. “Of the substrates used here, pyruvate/malate activates the chain at complex I, glutamate/malate and succinate at complexes II and III, ..” 2.2. Ponsot et al (2005) J Cell Physiol 203: 479-486. (a) Respiration (State 3) in permeabilized fibres with malate alone gave 25-50% of the flux with pyruvate+malate. This most likely indicates a large content of endogenous mitochondrial substrates, which interfere to an unknown degree with the kinetics of respiration after addition of exogenous substrates. In such a study, the conventional initial depletion of endogenous substrates would be most important. (b) Maximal respiration rates in muscle should be evaluated at saturating or high Pi, since at a Pi concentration of 3 mM OXPHOS respiration is phosphate limited. 2.3. Hulbert et al (2006) J Comp Physiol B 176: 93-105. Addition of ‘sparking malate concentrations’. This term can probably be derived from the misconception that tricarboxylic acid cycle intermediates are conserved during respiration of isolated mitochondria. 380 µM malate (instead of mM concentrations) in conjunction with 2.4 mM pyruvate were used, which makes a comparison difficult between different tissues and different species: the low malate concentration may limit PMP flux at various degrees in the different sources of mitochondria, and GMP may support higher fluxes than PMP at tissue- and species-specific degrees.

References Chapter 2

Chapter 3. Mitochondrial pathways to Complex II. Glycerophosphate dehydrogenase and electrontransferring flavoprotein

== Chapter 4. Mitochondrial pathways to Complexes I+II: Convergent electron transfer at the Q-Junction and additive effect of substrate combinations


== Chapter 5. Respiratory states, coupling control and coupling control ratios


== Chapter 6. Conversions of metabolic fluxes


Apendix

A1. Respiratory coupling states and coupling control ratios

A2. Substrates, uncouplers and inhibitors