1998
DOI: 10.1080/095530098142671
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Chromosomal instability in human lymphocytes after low dose rate gamma -irradiation and delayed mitogen stimulation

Abstract: Neither the acute genotoxic stress of HDR-irradiation compared with LDR-irradiation, nor the hypothesized conflict between mitogen-induced growth stimulation and irradiation-induced growth arrest, seem to be critical conditions for the development of chromosomal instability in primary human T lymphocytes. Post-irradiation incubation allowing apoptotic processes to remove damaged cells does not prevent the subsequent development of chromosomal instability during long-term cell proliferation.

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Cited by 31 publications
(11 citation statements)
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“…This is explained by the longer times available for DNA repair. Thus, increased clonogenic potential and lower yields of chromosome aberration [25] were observed in cells exposed to low-dose-rate irradiation. However, the effects of low dose rate on apoptosis are less clear [26] and an inverse dose rate effect has also been shown for lipid peroxidation [27], for radiation-induced damage of proteins and with the size of deletions at the HPRT locus [28].…”
Section: Dose Rate Effectmentioning
confidence: 99%
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“…This is explained by the longer times available for DNA repair. Thus, increased clonogenic potential and lower yields of chromosome aberration [25] were observed in cells exposed to low-dose-rate irradiation. However, the effects of low dose rate on apoptosis are less clear [26] and an inverse dose rate effect has also been shown for lipid peroxidation [27], for radiation-induced damage of proteins and with the size of deletions at the HPRT locus [28].…”
Section: Dose Rate Effectmentioning
confidence: 99%
“…Although genetic instability is normally associated with the high complexity of DNA damage caused by densely ionising radiation, chromosomal instability is also observed in X-and γ-irradiated cells [25,131,137].…”
Section: Genetic Instabilitymentioning
confidence: 99%
“…Thus, if the damage were repaired, the progeny of an irradiated cell would appear normal (Figure 1a), but if misrepaired, the progeny would be expected to show any transmissible radiation-induced genetic change and all cells derived from such a cell would exhibit the same genetic change, that is, the effect would be clonal ( Figure 1b). However, many laboratory studies have demonstrated nonclonal chromosome aberrations (Pampfer and Streffer, 1989;Kadhim et al, 1992Kadhim et al, , 1994Marder and Morgan, 1993;Holmberg et al, 1995Holmberg et al, , 1998Grosovsky et al, 1996;Watson et al, 2001) and mutations (Little et al, 1990(Little et al, , 1997Chang and Little, 1992;Harper et al, 1997) in the clonal progeny of irradiated cells. In addition, it has been apparent for many years that radiation-induced cytotoxicity, defined as loss of reproductive potential, may be delayed for up to six generations of cell replication (Puck and Marcus, 1956;Elkind and Sutton, 1959;Trott and Hug, 1970) with death occurring randomly among the progeny cells (Thompson and Suit, 1969).…”
mentioning
confidence: 99%
“…The principle genetic effect of an irradiation in low doses is radiation-induced genetic instability which lasts during numerous cell divisions after the initial cell has been irradiated (Holmberg et al 1998;McIlrath et al 2003). Genetic instability is favored by changes of repair activity, divergences in cell cycle control, and apoptosis (Murnane 1996).…”
Section: Discussionmentioning
confidence: 99%