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Cellular death after radiotherapy is delayed, some cells being capable of dividing up to 9 times before the clone dies.

.This cellular death seems to result from the progressive accumulation of chromosomal abnormalities with the various cell cycles, which results in a deficiency in the normal protein products of genes and a stopping of the metabolism, with a depletion of ATP storage and a perturbation of the mechanisms of ionic membrane transport: the cell dies by necrosis when it enters into mitosis.

Radiation can also provoke cellular death by apoptosis, between phases of the cell cycle, especially for lymphoma cells, but also for salivary and lachrymal gland cells and in the intestinal crypts.

The mechanisms involved in this apoptosis are relatively unknown: they could be the consequence of alterations of the cell membrane, with an elevation of intracellular calcium which would stimulate the nuclear calcium-dependant endonucleases.

The P-53 protein is a protective tumour suppressor gene: it induces apoptosis via protein P-21 or blocks the cell-cycle in G1 in order for the cell to repair the damage induced by radiation. After irradiation, an elevation of P-53 is observed, which can be either a symptom of cellular death by apoptosis or of cellular repair, according to the radiosensitivity mechanism of the cells (apoptosis or late necrosis).

The Bcl-2 gene protects against apoptosis by activating an antioxidising metabolic pathway and suppressing the lipid peroxidation produced within the cell by apoptotic signals.

PKC inhibits also the apoptotic cascade.

Numerous growth factors and cytokines are implied for inhibiting apoptosis via the activation of PKC, IGF-1 and α- FGF.