Respiration and Mitochondrial Membrane Potential Are not Required for Apoptosis and Anti-apoptotic Action of Bcl-2 in HeLa Cells

L. A. Shchepina¹, E. N. Popova², O. Yu. Pletjushkina², and B. V. Chernyak^2*

¹Department of Cell Physiology and Immunology, School of Biology, Lomonosov Moscow State University, Moscow, 119899 Russia

²Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, 119899 Russia; fax: (095) 939-3181; E-mail: bchernyak@yahoo.com

^* To whom correspondence should be addressed.

Received June 13, 2001; Revision received July 12, 2001

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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.

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KEY WORDS: apoptosis, necrosis, cytochrome c, mitochondria, respiration, membrane potential

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