Abstract
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 language | English |
|---|---|
| Pages (from-to) | 39-43 |
| Number of pages | 5 |
| Journal | Journal of Cerebral Blood Flow and Metabolism |
| Volume | 19 |
| Issue number | 1 |
| State | Published - Jun 30 1999 |
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Keywords
- Anoxia
- Apoptosis
- Ischemia
- Mitochondria
- Necrosis
- Permeability Transition pore
ASJC Scopus subject areas
- Endocrinology
- Neuroscience(all)
- Endocrinology, Diabetes and Metabolism
Cite this
Cytochrome c is released from mitochondria into the cytosol after cerebral anoxia or ischemia. / Perez-Pinzon, Miguel; Xu, Guang Ping; Born, James; Lorenzo, José; Busto, Raul; Rosenthal, Myron; Sick, Thomas.
In: Journal of Cerebral Blood Flow and Metabolism, Vol. 19, No. 1, 30.06.1999, p. 39-43.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cytochrome c is released from mitochondria into the cytosol after cerebral anoxia or ischemia
AU - Perez-Pinzon, Miguel
AU - Xu, Guang Ping
AU - Born, James
AU - Lorenzo, José
AU - Busto, Raul
AU - Rosenthal, Myron
AU - Sick, Thomas
PY - 1999/6/30
Y1 - 1999/6/30
N2 - 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.
AB - 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.
KW - Anoxia
KW - Apoptosis
KW - Ischemia
KW - Mitochondria
KW - Necrosis
KW - Permeability Transition pore
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UR - http://www.scopus.com/inward/citedby.url?scp=17444373424&partnerID=8YFLogxK
M3 - Article
C2 - 9886353
AN - SCOPUS:17444373424
VL - 19
SP - 39
EP - 43
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 1
ER -