Radiation induced cell cycle arrest: an overview of specific effects following high-LET exposure.
OBJECTIVE
Up to now only few studies on high LET radiation-induced cell cycle arrest are available. Open questions still remain concerning magnitude, persistence and control of the cell cycle inhibition after high-LET exposure. The intention of this review is to focus on the cell cycle distribution of the irradiated populations and the cell systems used (normal vs. mutant and tumor cells). The relevant published data are summarized.


CONCLUSIONS
Comparing isodoses, high-LET irradiation is a more potent inducer of cell cycle delays than low-LET irradiation. Generally, more pronounced delays in S- and G2-phase have been observed with increasing LET. The role of TP53 in relation to these effects is still controversial. A dose- and LET- dependent increase in cells arrested in G1-phase has as well been observed. Studies are presented indicating that a large fraction of normal fibroblasts irradiated in G1-phase and reseeded after exposure, did not re-enter the cell cycle but remained permanently arrested. The expression of cell cycle regulatory proteins in this case appeared more pronounced at high LET, but no fundamental differences were observed between low- and high-LET irradiation.
Fournier
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Department of Biophysics, GSI, Planckstr. 1, 64291 Darmstadt, Germany. c.fournier@gsi.de
Taucher-Scholz
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D002453:Cell Cycle / Q000528:radiation effects*; D018797:Cell Cycle Proteins / Q000096:biosynthesis; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D018499:Linear Energy Transfer; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53