The recent data on redox regulation of the mitochondrial cyclosporin-sensitive pore are reviewed here. They indicate that the pore is modulated by the redox state of pyridine nucleotides and glutathione at two independent sites. Special attention is paid to experimental approaches for studying this phenomenon in isolated mitochondria. The relation between oxidative stress and the opening of the mitochondrial pore in some cases of cell injury and in programmed cell death (apoptosis) is discussed.

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