Loss of Function of Cytochrome c in Jurkat Cells Undergoing Fas-mediated Apoptosis

Mitochondrial function was examined in Jurkat cells undergoing Fas-mediated apoptosis. With succinate or ascorbate/tetramethylphenylenediamine as substrate, oxygen uptake by digitonin-permeabilized apoptotic mitochondria was greatly decreased as compared with control. Assessment of the function of t...

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Bibliographic Details
Published in:The Journal of biological chemistry 1996-08, Vol.271 (35), p.21629-21636
Main Authors: Krippner, A, Matsuno-Yagi, A, Gottlieb, R A, Babior, B M
Format: Article
Language:English
Subjects:
Apoptosis - immunology
Cell Line
Cytochrome c Group - antagonists & inhibitors
Electron Transport
Endopeptidases - metabolism
Enzyme Activation
fas Receptor - physiology
Humans
Membrane Potentials - immunology
Mitochondria - enzymology
Mitochondria - physiology
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Summary:Mitochondrial function was examined in Jurkat cells undergoing Fas-mediated apoptosis. With succinate or ascorbate/tetramethylphenylenediamine as substrate, oxygen uptake by digitonin-permeabilized apoptotic mitochondria was greatly decreased as compared with control. Assessment of the function of the cytochrome c -cytochrome oxidase segment of the electron transport chain of apoptotic mitochondria showed that the activity of cytochrome oxidase appeared to be normal, but that of cytochrome c was greatly diminished. A death protease was found to participate in the events leading to the loss of cytochrome c activity, but the cytochrome did not seem to be extensively degraded during the course of apoptosis. Our results suggest that a rapid loss in mitochondrial function due at least in part to the inhibition or inactivation of cytochrome c is a potentially fatal component of the apoptosis program of Jurkat cells.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.271.35.21629