Mitochondria, Oxygen and Reperfusion Damage

Abstract

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.

Key Words:

• reperfusion damage
• mitochondria
• calcium
• cyclosporin
• oxidative stress