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. 1999 Nov 15;147(4):809–822. doi: 10.1083/jcb.147.4.809

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© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Model of two types of mitochondrial outer membrane permeability observed in Xenopus extracts during apoptosis. Mitochondria treated with tBid or Bax in buffer undergo efflux of endogenous cytochrome c (12 pmol/μl mitochondria) across the outer membrane, with limited permeability to exogenous cytochrome c. Additional exposure to cytosol (PEF) allows high permeability to exogenous cytochrome c (60 nmol/μl mitochondria per min, as measured by the rate of the complex IV reaction). Thus, this increased exchange of endogenous cytochrome c is at least ∼5,000 times the rate of cytochrome c efflux after tBid or Bax treatment, assuming that all of the mitochondrial cytochrome c is released over 1 min. PEF begins to act immediately after tBid–induced permeabilization, but is inactivated over 1–2 h by caspase activation. The inner membrane appears unaffected.