Investigation of Calcium Accumulation in Mitochondria in Cells Undergoing Apoptosis

V. E. Galitovsky and V. G. Gogvadze^*

Institute of Theoretical and Experimental Biophysics, Pushchino, Moscow Region, 142290 Russia; fax: (096) 779-0553; E-mail: vlad_gogvadze@hotmail.com

^* To whom correspondence should be addressed.

Received September 22, 2000; Revision received October 17, 2000

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One of the earliest features of apoptosis is the induction of the mitochondrial permeability transition (MPT) due to opening of a pore in the mitochondrial membrane. We estimated the Ca²⁺ capacity of mitochondria (a threshold level of Ca²⁺ that induces the release of this cation from mitochondria) during apoptosis. Incubation of thymocytes at 37°C for 4 h equally decreased the mitochondrial Ca²⁺ capacity both in the presence and the absence of dexamethasone, an inducer of apoptosis. At the same time, dexamethasone significantly stimulated internucleosomal DNA fragmentation, which is one of the manifestations of apoptosis. Cyclosporin A prevented the time-dependent decrease in the Ca²⁺ capacity of mitochondria but did not affect internucleosomal DNA fragmentation. Therefore, induction of apoptosis assessed by internucleosomal DNA fragmentation is not mediated by the mitochondrial permeability transition.

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KEY WORDS: apoptosis, mitochondria, calcium, permeability transition

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