Difference between revisions of "Gnaiger 1998 BTK-COX"

From Bioblast
Jump to navigation Jump to search
Line 4: Line 4:
|year=1998
|year=1998
|mipnetlab=AT_Innsbruck_GnaigerE
|mipnetlab=AT_Innsbruck_GnaigerE
|abstract=Metabolic rate is regulated by a hierarchy of behavioural, physiological and biochemical mechanisms in the dynamic range between minimum and maximum activity of an organism. Such regulation operates at time scales as low as seconds, e.g. in rest-work transitions of muscle. Biochemical regulation of metabolic flux represents a classical topic of enzyme kinetics, relating to down-regulation of key enzymes in metabolic pathways (e.g. [1]) and upregulation of enzyme cascades. On the other hand, control of metabolic capacity for maximum
|abstract=Metabolic rate is regulated by a hierarchy of behavioural, physiological and biochemical mechanisms in the dynamic range between minimum and maximum activity of an organism. Such regulation operates at time scales as low as seconds, e.g. in rest-work transitions of muscle. Biochemical regulation of metabolic flux represents a classical topic of enzyme kinetics, relating to down-regulation of key enzymes in metabolic pathways (e.g. [1]) and upregulation of enzyme cascades. On the other hand, control of metabolic capacity for maximum flux is distributed over a large number of steps, as studied with the tool of flux control analysis [2,3]. Enzyme capacities and distribution of control change over the life span during development and ageing, by acclimation and pathological defects. Biochemical adaptations yield distinct metabolic strategies under selective pressure over evolutionary time [4]. Evolutionary optimisation of organismic form and function results in matched capacities for oxygen supply to mitochondria in the respiratory cascade and respiratory capacity of mitochondria, as summarised by the concept of symmorphosis [5,6] (Fig. 1). With the exception of excessive lung structure, such close matching is actually observed [6,7]. In the mitochondrial respiratory chain, however, cytochrome c oxidase appears to be expressed in excess over the capacity for mitochondrial oxygen flux [7-10]. Here we report results on oxygen kinetics in isolated mitochondria and cytochrome c oxidase, (i) providing a new perspective on the respiratory cascade and symmorphosis by relating mitochondrial oxygen affinity to intracellular oxygen pressure, and (ii) proposing a functional role of excess capacity of cytochrome c oxidase in terms of “synkinetic” regulation of high mitochondrial oxygen affinity.
flux is distributed over a large number of steps, as studied with the tool of flux control analysis [2,3]. Enzyme capacities and distribution of control change over the life span during development and ageing, by acclimation and pathological defects. Biochemical adaptations yield distinct metabolic strategies under selective pressure over evolutionary time [4]. Evolutionary optimisation of organismic form and function results in matched capacities for oxygen supply to mitochondria in the respiratory cascade and respiratory capacity of mitochondria, as summarised by the concept of symmorphosis [5,6] (Fig. 1). With the exception of excessive lung structure, such close matching is actually observed [6,7]. In the mitochondrial respiratory chain, however, cytochrome c oxidase appears to be expressed in excess over the capacity for mitochondrial oxygen flux [7-10]. Here we report results on oxygen kinetics in isolated mitochondria and cytochrome c oxidase, (i) providing a new perspective on the respiratory cascade and symmorphosis by relating mitochondrial oxygen affinity to intracellular oxygen pressure, and (ii) proposing a functional role of excess capacity of cytochrome c oxidase in terms of “synkinetic” regulation of high mitochondrial oxygen affinity.
}}
}}
{{Labeling
{{Labeling

Revision as of 20:28, 13 September 2010

Publications in the MiPMap
Gnaiger E, Kuznetsov AV, Lassnig B, Margreiter R (1998) Functional interpretation of the flux control coefficient and excess capacity of cytochrome c oxidase at intracellular oxygen. In BioThermo-Kinetics in the Post Genomic Era (Larsson C, Påhlman I-L, Gustafsson L, eds) Chalmers Reproservice, Göteborg: 81-88.


Gnaiger E, Kuznetsov AV, Lassnig B, Margreiter R (1998)

Abstract: Metabolic rate is regulated by a hierarchy of behavioural, physiological and biochemical mechanisms in the dynamic range between minimum and maximum activity of an organism. Such regulation operates at time scales as low as seconds, e.g. in rest-work transitions of muscle. Biochemical regulation of metabolic flux represents a classical topic of enzyme kinetics, relating to down-regulation of key enzymes in metabolic pathways (e.g. [1]) and upregulation of enzyme cascades. On the other hand, control of metabolic capacity for maximum flux is distributed over a large number of steps, as studied with the tool of flux control analysis [2,3]. Enzyme capacities and distribution of control change over the life span during development and ageing, by acclimation and pathological defects. Biochemical adaptations yield distinct metabolic strategies under selective pressure over evolutionary time [4]. Evolutionary optimisation of organismic form and function results in matched capacities for oxygen supply to mitochondria in the respiratory cascade and respiratory capacity of mitochondria, as summarised by the concept of symmorphosis [5,6] (Fig. 1). With the exception of excessive lung structure, such close matching is actually observed [6,7]. In the mitochondrial respiratory chain, however, cytochrome c oxidase appears to be expressed in excess over the capacity for mitochondrial oxygen flux [7-10]. Here we report results on oxygen kinetics in isolated mitochondria and cytochrome c oxidase, (i) providing a new perspective on the respiratory cascade and symmorphosis by relating mitochondrial oxygen affinity to intracellular oxygen pressure, and (ii) proposing a functional role of excess capacity of cytochrome c oxidase in terms of “synkinetic” regulation of high mitochondrial oxygen affinity.


O2k-Network Lab: AT_Innsbruck_GnaigerE


Labels:

Stress:Hypoxia  Organism: Rat  Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property., Hepatocyte; Liver"Hepatocyte; Liver" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.  Preparation: 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., Oxidase; Biochemical Oxidation"Oxidase; Biochemical Oxidation" 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., Enzyme 

Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" 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., Flux Control; Additivity; Threshold; Excess Capacity"Flux Control; Additivity; Threshold; Excess Capacity" 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., Substrate; Glucose; TCA Cycle"Substrate; Glucose; TCA Cycle" 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. 


HRR: Oxygraph-2k