Mechanism of cell damage in brain ischemia: a hypothesis.
Mitochondria are known to develop a series of abnormalities as a result of ischemia. The inability of mitochondria to resume normal function following reperfusion has been implicated as an important factor in irreversible cell damage. However, the mechanism of mitochondrial injury after ischemic brain insult is poorly understood. In this paper a hypothesis is proposed which concentrates on the interrelated roles of phosphate, calcium, and electron transport on ischemic brain cell injury.
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D002118:Calcium / Q000502:physiology; D004579:Electron Transport; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D010710:Phosphates / Q000502:physiology
D010710:Phosphates; D002118:Calcium