New evidence suggests that physiological and damaging agents activate two different pathways of apoptotic signalling, which are mediated by protein-protein interactions and mitochondrial alterations respectively. The two pathways converge at the activation of caspase 3, the key effector of the execution phase of apoptosis, thus giving similar final results. The knowledge that different biochemical routes exist allows us to re-evaluate previous apparently contradictory results concerning the events occurring during apoptosis, and their respective roles. In particular, this applies to the role of oxidative stress and redox imbalance in the signal transduction events of apoptosis. It now appears that oxidative alterations are absent, or at least unnecessary, for the development of the physiological pathway. Instead, clear indications are emerging showing that redox imbalance is required for the damage-induced mitochondrial pathway. This is suggested by the finding that the depletion of glutathione, a common event in damage-induced apoptosis, is necessary and sufficient to induce cytochrome c release, the key event of this pathway. A model is proposed with GSH efflux as the backbone of the damage-induced apoptotic pathway.
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Conference Article|
February 01 2000
GSH extrusion and the mitochondrial pathway of apoptotic signalling
S. Coppola;
S. Coppola
1Dipartimento di Biologia, Università di Tor Vergata, via delle Ricerca Scientifica, 00133 Roma, Italy
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L. Ghibelli
L. Ghibelli
1
1Dipartimento di Biologia, Università di Tor Vergata, via delle Ricerca Scientifica, 00133 Roma, Italy
1To whom correspondence should be addressed.
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Publisher: Portland Press Ltd
Received:
August 06 1999
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2000 Biochemical Society
2000
Biochem Soc Trans (2000) 28 (2): 56–61.
Article history
Received:
August 06 1999
Citation
S. Coppola, L. Ghibelli; GSH extrusion and the mitochondrial pathway of apoptotic signalling. Biochem Soc Trans 1 February 2000; 28 (2): 56–61. doi: https://doi.org/10.1042/bst0280056
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