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Regulation of in Vivo Mitochondrial Oxidative Phosphorylation

  • David F. Wilson

Abstract

The regulation of mitochondrial respiration in vivo is designed to maintain a supply of cellular ATP under conditions for which its hydrolysis is sufficiently energetic to do the required metabolic work. In vivo, various metabolic pathways in the mitochondrial matrix (citric acid cycle, fatty acid oxidation, etc.) contain dehydrogenases, which catalyze the transfer of reducing equivalents from substrates to NAD+ and FAD to form NADH and FADH2. These coenzymes are then reoxidized by the respiratory chain, serving as the source of the reducing equivalents that reduce molecular oxygen to water. The amounts of NADH and FADH2 available to the respiratory chain are determined by the metabolic pathways being utilized, but in general, NADH provides most of the total reducing equivalents. Metabolic regulation ensures that these equivalents (NAD couple) are available at a relatively constant oxidation-reduction potential (from −240 mV to −280 mV depending on cell type and metabolic status). This differs markedly from the conditions normally utilized for evaluation of the regulation of mitochondrial functions in suspensions of isolated mitochondria. In the latter case, reducing substrate is added in excess and the potential of the NAD couple can be as negative as −350 mV. This is one of the reasons care must be exercised in extrapolating from in vitro measurements to in vivo function.

Keywords

Respiratory Rate Oxidative Phosphorylation Adenine Nucleotide Citric Acid Cycle Mitochondrial Oxidative Phosphorylation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • David F. Wilson
    • 1
  1. 1.Department of Biochemistry and BiophysicsUniversity of PennsylvaniaPhiladelphiaUSA

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