Radiation-induced genomic instability in repair deficient mutants of Chinese hamster cells.
OBJECTIVE
To determine the role of single (SSB) and double strand break (DSB) repair in the induction and propagation of radiation-induced instability.


METHODS
Two defined hamster cell lines with known DNA repair deficiencies in DSB repair (XR-C1) and base excision repair (EM-C11) and the parental wild-type line (CHO-9) were used. The rate of micronucleus formation, apoptosis and survival were measured at 0, 7 and 14 days after X-ray radiation.


RESULTS
An enhanced rate of production of damaged cells was observed in wild type and the repair deficient mutants after irradiation. This was cell type, dose and time-dependent. All cells demonstrated delayed death up to day 14 after irradiation along with an elevated apoptosis frequency. The yield of micronuclei was not significantly increased in the wild-type cells, but was in the mutant cells, over the dose and time range studied. For all three endpoints the increase in damage was most pronounced in the SSB deficient cell line.


CONCLUSIONS
SSB and/or oxidized base damage play a major role, rather than DSB, in radiation induced instability.
Somodi
Zsolt
Z
Gray Cancer Institute, Northwood, Middlesex, UK.
Zyuzikov
Nikolay A
NA
Kashino
Genro
G
Trott
Klaus-R
KR
Prise
Kevin M
KM
D000818:Animals; D017209:Apoptosis; D016466:CHO Cells; D016923:Cell Death; D006224:Cricetinae; D004247:DNA; D004260:DNA Repair / Q000235:genetics*; D004277:DNA, Single-Stranded; D042822:Genomic Instability / Q000528:radiation effects*; D015162:Micronucleus Tests; D018384:Oxidative Stress; D011832:Radiation Injuries / Q000235:genetics*
D004277:DNA, Single-Stranded; D004247:DNA