Abstract
Apoptosis is thought to be a programmed form of cell death which, when balanced by cell proliferation, contributes to the regulation of tissue homeostasis (1). An imbalance between apoptosis and proliferation may be a factor in tumorigenesis. Apoptosis differs from necrosis both morphologically and biochemically. Necrotic cells exhibit an early loss of the ionic gradient across the cell membrane and non-cell cycle dependent random DNA degradation subsequent to release of lysosomal enzymes (1, 2). in contrast, cells dying by apoptosis maintain ionic gradients and characteristically exhibit internucleosomal DNA fragmentation (IDF) before the loss of cell membrane integrity occurs (3). IDF results from the activation of a nuclear, Ca2+/Mg2+ dependent or pH sensitive endonuclease, possibly DNase I or II (4). Apoptosis appears to be related to arrest of the cell cycle (3, 5, 6). Induction of apoptosis often requires a proliferative stimulus and can be thought of as process of abortive mitosis.
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Patierno, S.R., Blankenship, L.J., Wise, J.P., Xu, J., Bridgewater, L.C., Manning, F.C.R. (1994). Genotoxin-Induced Apoptosis: Implications for Carcinogenesis. In: Hu, V.W. (eds) The Cell Cycle. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2421-2_39
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DOI: https://doi.org/10.1007/978-1-4615-2421-2_39
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