Reparable and non-reparable DNA strand breaks induced by X-irradiation in CHO K1 cells and the radiosensitive mutants xrs1 and xrs5.
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Reparable and non-reparable DNA strand breaks induced by X-irradiation in CHO K1 cells and the radiosensitive mutants xrs1 and xrs5. / Dahm-Daphi, Jochen; Dikomey, E; Pyttlik, C; Jeggo, P A.
in: INT J RADIAT BIOL, Jahrgang 64, Nr. 1, 1, 1993, S. 19-26.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Reparable and non-reparable DNA strand breaks induced by X-irradiation in CHO K1 cells and the radiosensitive mutants xrs1 and xrs5.
AU - Dahm-Daphi, Jochen
AU - Dikomey, E
AU - Pyttlik, C
AU - Jeggo, P A
PY - 1993
Y1 - 1993
N2 - Repair kinetics of X-ray-induced DNA lesions was measured for CHO K1, xrs1 and xrs5 cells using the alkaline unwinding technique. Cells were irradiated on ice with X-ray doses of 9, 30 and 90 Gy followed by repair incubation at 37 degrees C. Repair was studied for up to 60 h to cover the kinetics of reparable and non-reparable DNA damage. The kinetics of single-strand break (ssb) repair was found to be the same in CHO K1 and xrs cells. In contrast, the number of double-strand breaks (dsbs) was shown to decline with half-times that were longer for xrs1 and xrs5 as compared with CHO K1 cells (12.2 and 15.0 h versus 4.9 h for 90 Gy). These differences are primarily due to differences in the fraction of non-reparable dsbs which was higher by a factor of 3-4 for xrs1 and xrs5 cells as compared with K1 cells (3.2 and 3.7% versus 1.0% for 90 Gy). However, the kinetics of those dsbs which were actually repaired did not show any significant differences for the three cell lines studied and were rejoined at a mean half-time of 3.8 h. It is suggested that the higher number of non-reparable breaks in xrs cells may not be attributable to a deficient enzymatic repair system. It is suggested that alterations in chromatin conformation might prevent rejoining of a portion of dsbs.
AB - Repair kinetics of X-ray-induced DNA lesions was measured for CHO K1, xrs1 and xrs5 cells using the alkaline unwinding technique. Cells were irradiated on ice with X-ray doses of 9, 30 and 90 Gy followed by repair incubation at 37 degrees C. Repair was studied for up to 60 h to cover the kinetics of reparable and non-reparable DNA damage. The kinetics of single-strand break (ssb) repair was found to be the same in CHO K1 and xrs cells. In contrast, the number of double-strand breaks (dsbs) was shown to decline with half-times that were longer for xrs1 and xrs5 as compared with CHO K1 cells (12.2 and 15.0 h versus 4.9 h for 90 Gy). These differences are primarily due to differences in the fraction of non-reparable dsbs which was higher by a factor of 3-4 for xrs1 and xrs5 cells as compared with K1 cells (3.2 and 3.7% versus 1.0% for 90 Gy). However, the kinetics of those dsbs which were actually repaired did not show any significant differences for the three cell lines studied and were rejoined at a mean half-time of 3.8 h. It is suggested that the higher number of non-reparable breaks in xrs cells may not be attributable to a deficient enzymatic repair system. It is suggested that alterations in chromatin conformation might prevent rejoining of a portion of dsbs.
M3 - SCORING: Zeitschriftenaufsatz
VL - 64
SP - 19
EP - 26
JO - INT J RADIAT BIOL
JF - INT J RADIAT BIOL
SN - 0955-3002
IS - 1
M1 - 1
ER -