Biologia, Bratislava 54/Suppl. 6: 21-27, 1999.

ISSN 0006-3088 (Biologia). ISSN 1335-6399 (Biologia. Section Cellular and Molecular Biology).

 

Review

Calcium and mitochondria in ischemic cell death.

 

Tibor Kristian* & Bo K. Siesjo

Center for the Study of Neurological Disease, The Queen´s Medical Center, 1356 Lusitana street, UH Tower 8th floor, Honolulu, Hawaii 96813, USA; fax: ++1 808 537 7899, e-mail: tibor@cns.queens.org

* corresponding author

Received: December 28, 1998 / Accepted: October 5, 1999

 

Abstract

Ischemia is accompanied by mitochondrial dysfunction leading to a fall in ATP concentration and phosphorylation potential, and to loss of cellular ion homeostasis. The ensuing rise in intracellular calcium concentration caused by bioenergetical failure is believed to be harmful to cells. Following brief ischemic insults, mitochondrial function is usually normalized in the early reperfusion period and ion concentration gradients are restored. However reperfusion, especially following long-lasting ischemic periods, may be accompanied by secondary mitochondrial failure, which can trigger a lethal cascade of events known as apoptosis, or cause necrotic cell death. There is accumulating evidence that mitochondrial dysfunction plays a pivotal role in this cascade. This has led to an intense search for conditions and factors which trigger such dysfunction, particularly that devoted the mitochondrial permeability transition.

 

Key words: ischemia, mitochondria, calcium, free radicals, apoptosis, necrosis.