Cytochrome c is released from mitochondria into the cytosol after cerebral anoxia or ischemia

Miguel A. Pérez-Pinzón, Guang Ping Xu, James Born, José Lorenzo, Raul Busto, Myron Rosenthal, Thomas J. Sick

Research output: Contribution to journalArticlepeer-review

114 Scopus citations


Mitochondrial dysfunction may underlie both acute and delayed neuronal cell death resulting from cerebral ischemia. Specifically, postischemic release of mitochondrial constituents such as the pro-apoptotic respiratory chain component cytochrome c could contribute acutely to further mitochondrial dysfunction and to promote delayed neuronal death. Experiments reported here tested the hypothesis that ischemia or severe hypoxia results in release of cytochrome c from mitochondria. Cytochrome c was measured spectrophotometrically from either the cytosolic fraction of cortical brain homogenates after global ischemia plus reperfusion, or from brain slices subjected to severe hypoxia plus reoxygenation. Cytochrome c content in cytosol derived from cerebral cortex was increased after ischemia and reperfusion. In intact hippocampal slices, there was a loss of reducible cytochrome c after hypoxia/reoxygenation, which is consistent with a decrease of this redox carrier in the mitochondrial pool. These results suggest that cytochrome c is lost to the cytosol after cerebral ischemia in a manner that may contribute to postischemic mitochondrial dysfunction and to delayed neuronal death.

Original languageEnglish (US)
Pages (from-to)39-43
Number of pages5
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number1
StatePublished - 1999


  • Anoxia
  • Apoptosis
  • Ischemia
  • Mitochondria
  • Necrosis
  • Permeability Transition pore

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism


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