JBC INTERFERin siRNA transfection reagent

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Studies on the Electron Transfer System

LXVI. EFFECT OF DIPHOSPHOPYRIDINE NUCLEOTIDE DEFICIENCY ON RESPIRATION, RESPIRATORY CONTROL, AND PHOSPHORYLATION IN MITOCHONDRIA

David H. MacLennan 1 and Alexander Tzagoloff 1

From the 1 From the Institute for Enzyme Research, University of Wisconsin, Madison, Wisconsin 53706

Mitochondria which have been depleted of their pyridine nucleotides by aging at 38°, and are essentially devoid of the ability to oxidize diphosphopyridine nucleotide-linked substrates, recover a large part of their oxidative capacity after exposure to adenosine 5'-triphosphate and magnesium chloride. Such reconstituted mitochondria have only 10 to 20% of the initial concentration of DPN+, but the rates of oxidation, with pyruvate plus malate as substrate, are nearly maximal. Such mitochondria are also capable of carrying out oxidative phosphorylation with high efficiency and have respiratory control ratios between 3 and 6. These findings indicate that maximal rates of oxidation and phosphorylation are compatible with amounts of DPN+ that are no higher than those of the fixed component of the chain (1.2 mµmoles per mg of protein or less).

Submitted on October 18, 1965


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