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Radiation-Induced Cell Death and its Implications in Human Disease

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Part of the book series: Results and Problems in Cell Differentiation ((RESULTS,volume 24))

Abstract

Exposure of cells to ionizing radiation leads to a variety of damages to DNA including those that arise as a consequence of direct interaction and those that arise indirectly due to radiolysis of water which generates aqueous electrons, hydrogen atoms and hydroxyl radicals (Ward 1975). As with other DNA damaging agents the damage may be repaired, thus maintaining the fidelity of DNA after cell division; misrepair may occur leading to gene mutation and possibly cell transformation or if the extent of the damage is sufficiently great the cell may die from apoptosis or necrosis (Weichselbaum et al. 1976; Smith et al. 1980). However, the cellular radiation response is more complex than simply responding to DNA damage by repairing lesions. It is now evident that a number of signalling pathways can be activated in response to radiation damage involving both the activation or inactivation of existing proteins as well as the induction of a number of genes (Fornace 1992; Knebel et al. 1996). Some of these pathways are activated in response to DNA damage, but signalling is not exclusively initiated by such lesions since it has been demonstrated that membrane receptors can mediate the transmission of such signals (Karin and Hunter 1995). Signals initiated in these pathways can elicit DNA repair, lead to cell cycle arrest or direct cells to undergo apoptosis.

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Lavin, M.F. (1998). Radiation-Induced Cell Death and its Implications in Human Disease. In: Kumar, S. (eds) Apoptosis: Mechanisms and Role in Disease. Results and Problems in Cell Differentiation, vol 24. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-69185-3_10

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