We have examined the ultrastructure of mitochondria as it relates to energy metabolism in the intact cell. Oxidative phosphorylation was induced in ultrastructurally intact Ehrlich ascites tumor cells by rapidly generating intracellular adenosine diphosphate from endogenous adenosine triphosphate by the addition of 2-deoxyglucose. The occurrence of oxidative phosphorylation was ascertained indirectly by continuous and synchronous monitoring of respiratory rate, fluorescence of pyridine nucleotide, and 90° light-scattering. Oxidative phosphorylation was confirmed by direct enzymatic analysis of intracellular adenine nucleotides and by determination of intracellular inorganic orthophosphate. Microsamples of cells rapidly fixed for electron microscopy revealed that, in addition to oxidative phosphorylation, an orthodox → condensed ultrastructural transformation occurred in the mitochondria of all cells in less than 6 sec after the generation of adenosine diphosphate by 2-deoxyglucose. A 90° light-scattering increase, which also occurs at this time, showed a t ½ of only 25 sec which agreed temporally with a slower orthodox → maximally condensed mitochondrial transformation. Neither oxidative phosphorylation nor ultrastructural transformation could be initiated in mitochondria in intact cells by the intracellular generation of adenosine diphosphate in the presence of uncouplers of oxidative phosphorylation. Partial and complete inhibition of oxidative phosphorylation by oligomycin resulted in a positive relationship to partial and complete inhibition of 2-deoxyglucose-induced ultrastructural transformation in the mitochondria in these cells. The data presented reveal that an orthodox → condensed ultrastructural transformation is linked to induced oxidative phosphorylation in mitochondria in the intact ascites tumor cell.
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1 October 1971
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October 01 1971
OXIDATIVE PHOSPHORYLATION AND ULTRASTRUCTURAL TRANSFORMATION IN MITOCHONDRIA IN THE INTACT ASCITES TUMOR CELL
Charles R. Hackenbrock,
Charles R. Hackenbrock
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
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Terry G. Rehn,
Terry G. Rehn
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
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Eugene C. Weinbach,
Eugene C. Weinbach
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
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John J. Lemasters
John J. Lemasters
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
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Charles R. Hackenbrock
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
Terry G. Rehn
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
Eugene C. Weinbach
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
John J. Lemasters
From the Department of Anatomy, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.
Dr. Hackenbrock's present address is the Department of Cell Biology, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Received:
January 21 1971
Revision Received:
May 03 1971
Online ISSN: 1540-8140
Print ISSN: 0021-9525
Copyright © 1971 by The Rockefeller University Press
1971
J Cell Biol (1971) 51 (1): 123–137.
Article history
Received:
January 21 1971
Revision Received:
May 03 1971
Citation
Charles R. Hackenbrock, Terry G. Rehn, Eugene C. Weinbach, John J. Lemasters; OXIDATIVE PHOSPHORYLATION AND ULTRASTRUCTURAL TRANSFORMATION IN MITOCHONDRIA IN THE INTACT ASCITES TUMOR CELL . J Cell Biol 1 October 1971; 51 (1): 123–137. doi: https://doi.org/10.1083/jcb.51.1.123
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