Abstract
The release of cytochrome c from intermembrane space of mitochondria into cytosol is one of the critical events in apoptotic cell death. The important anti-apoptotic oncoprotein Bcl-2 inhibits this process. In the present study it was shown that apoptosis and release of cytochrome c induced by staurosporine or by tumor necrosis factor-alpha in HeLa cells were not affected by inhibitors of respiration (rotenone, myxothiazol, antimycin A) or by uncouplers (CCCP, DNP) that decrease the membrane potential at the inner mitochondrial membrane. The inhibitors of respiration and the uncouplers did not affect also the anti-apoptotic activity of Bcl-2.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antifungal Agents / pharmacology
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Antimycin A / pharmacology
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Apoptosis*
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Carbonyl Cyanide m-Chlorophenyl Hydrazone / pharmacology
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Cell Respiration / physiology
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Cytochrome c Group / metabolism*
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Genetic Vectors
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HeLa Cells / metabolism*
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Humans
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Membrane Potentials / physiology
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Methacrylates
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Mitochondria / drug effects
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Mitochondria / enzymology*
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Proto-Oncogene Proteins c-bcl-2 / physiology*
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Rotenone / pharmacology
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Signal Transduction / physiology
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Staurosporine / pharmacology
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Thiazoles / pharmacology
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Transfection
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Uncoupling Agents / pharmacology
Substances
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Antifungal Agents
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Cytochrome c Group
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Methacrylates
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Proto-Oncogene Proteins c-bcl-2
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Thiazoles
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Uncoupling Agents
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Rotenone
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Carbonyl Cyanide m-Chlorophenyl Hydrazone
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Antimycin A
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myxothiazol
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Staurosporine