Ma. Perez-pinzon et al., Cytochrome C is released from mitochondria into the cytosol after cerebralanoxia or ischemia, J CEREBR B, 19(1), 1999, pp. 39-43
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 dy
sfunction 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 spectrophotometr
ically from either the cytosolic fraction of cortical brain homogenates aft
er global ischemia plus reperfusion, or from brain slices subjected to seve
re hypoxia plus reoxygenation. Cytochrome c content in cytosol derived from
cerebral cortex was increased after ischemia and reperfusion. In intact hi
ppocampal 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 pos
tischemic mitochondrial dysfunction and to delayed neuronal death.