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Apoptosis — Searching for the Central Executioner

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Part of the book series: Ernst Schering Research Foundation Workshop ((3368,volume 6))

Abstract

Apoptosis may be defined as a regulated lethal process in which the cell activates catabolic processes which, within the limits of a near-to-intact plasma membrane, lead to a stereotyped ensemble of biochemical and morphological alterations. Such alterations include a reduction in cell size, a condensation of chromatin, and changes in the physicochemistry of the plasma membrane facilitating the recognition and heterophagic removal of the apoptotic cell by adjacent normal cells. The most striking morphological change in apoptotic cells concerns the nucleus which invariably exhibits chromatin condensation, mostly associated with enzymatic degradation of nuclear DNA. However, chromatin condensation is a sign of apoptosis rather than a mechanism leading to cell death, since non-nuclear apoptosis-associated alterations can be induced in anucleate cells (cytoplasts), as this has been shown in 1994 (Jacobson et al. 1994, Schulze-Osthoff et al. 1994).

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Abbreviations

BA:

bongkrekic acid

CsA:

cyclosporin A

ΔΨm :

mitochondrial transmenbrane potential

PTPC:

permeability transition pore complex

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© 2000 Springer-Verlag Berlin Heidelberg

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Daugas, E., Kroemer, G. (2000). Apoptosis — Searching for the Central Executioner. In: Jégou, B., Pineau, C., Saez, J. (eds) Testis, Epididymis and Technologies in the Year 2000. Ernst Schering Research Foundation Workshop, vol 6. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-04050-8_9

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  • DOI: https://doi.org/10.1007/978-3-662-04050-8_9

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-04052-2

  • Online ISBN: 978-3-662-04050-8

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