Mitochondria, oxygen and reperfusion damage.
Reperfusion of the ischaemic or hypoxic heart elicits a number of oxygen dependent processes such as cell lysis and Ca2+ uptake. It is known that the energisation of mitochondria, which requires oxygen, plays a key role in these processes and that the organelle actively sequesters Ca2+ under these circumstances. In this brief review we discuss how oxidants derived from mitochondrial electron transport may perturb mitochondrial calcium handling on reoxygenation of the hypoxic myocardium. In addition we show that the immunosuppressive agent cyclosporin has little or no effect on the oxygen dependent increase in total cell Ca2+ which occurs when hypoxic myocytes are reoxygenated. This result suggests that the Ca2+ dependent mitochondrial pore, which is known to function under conditions of oxidative stress, does not play a major role in the perturbation of Ca2+ homeostasis which occurs on reoxygenation of hypoxic hearts.
Darley-Usmar
V M
VM
Department of Biochemical Sciences, Wellcome Research Laboratories, Beckenham, Kent U.K.
Stone
D
D
Smith
D
D
Martin
J F
JF
D000255:Adenosine Triphosphate / Q000378:metabolism; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism*; D015687:Cell Hypoxia / Q000502:physiology; D016572:Cyclosporine / Q000494:pharmacology; D006706:Homeostasis; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology
D016572:Cyclosporine; D000255:Adenosine Triphosphate; D002118:Calcium