Gnaiger 1998 BTK-COX

From Bioblast
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, PΓ₯hlman I-L, Gustafsson L, eds) Chalmers Reproservice, GΓΆteborg:81-8.

Gnaiger Erich, Kuznetsov AV, Lassnig B, Margreiter R (1998) Chalmers Reproservice

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 β€œsynkinetic” regulation of high mitochondrial oxygen affinity.

β€’ O2k-Network Lab: AT Innsbruck Gnaiger E


Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Heart, Liver  Preparation: Isolated mitochondria, Enzyme, Oxidase;biochemical oxidation 

Regulation: Substrate  Coupling state: OXPHOS 

HRR: Oxygraph-2k 

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