Studies on the subcellular pathophysiology of ischemia.
The loss of ability to synthesize adenosine triphosphate (ATP) by mitochondria in ischemic cells even in a favorable medium correlates with the loss of cell viability. The early lesion at the molecular level needs further investigation but appears to involve an increased permeability of the mitochondrial membrane possibly promoting proton leak and obviating oxidative phosphorylation. The nature of this leak could involve changes in phospholipid-protein interactions, especially since the early release of free fatty acids and changes in phospholipid composition occur.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D002118:Calcium / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism* / Q000473:pathology; D004285:Dogs; D007668:Kidney / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism* / Q000648:ultrastructure; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure; D010539:Permeability; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism
D000255:Adenosine Triphosphate; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium