REPAIR OF RADIATION-INDUCED CHROMATID ABERRATIONS - RELATIONSHIP TO G2 ARREST IN CHO CELLS

被引:11
|
作者
ROWLEY, R
机构
[1] Experimental Oncology, Department of Radiology, University of Utah Medical Center, Salt Lake City, UT
关键词
D O I
10.1080/09553009014551831
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The literature suggests that the function of radiation-induced G2 arrest is to allow repair of potentially lethal damage before cell-entry into, and damage expression in, mitosis. The nature of the damage repaired is not known, but chromosome aberrations have been considered. To examine this possibility in G2 cells, the rate of repair of chromatid aberrations in CHO cells progressing to or arrested in G2 was compared with the rate of repair of the damage which gives rise to G2 arrest. To measure aberration repair rates, exponentially growing CHO cells arrested in G2 with 1.5, 2.5 or 3.5 Gy of X-rays were released into mitosis by treatment with 5 mm caffeine immediately or 1, 2 or 3 h after irradiation. Aberration frequencies in these cells were then related to the caffeine-free (repair) interval. To measure the rate of repair of arrest-causing damage a split-dose procedure was used. The half-times for aberration repair were approximately 1 h for achromatic gaps and 1.5 h for breaks, intrachanges and interchanges. The half-time for arrest damage repair varied with radiation dose. This result suggests that chromatid aberrations are not a primary cause of radiation-induced G2 arrest. © 1990 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.
引用
收藏
页码:489 / 498
页数:10
相关论文
共 50 条
  • [31] Hip2 ubiquitin-conjugating enzyme overcomes radiation-induced G2/M arrest
    Bae, Yoonhee
    Jung, Song Hwa
    Kim, Goo-Young
    Rhim, Hyangshuk
    Kang, Seongman
    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2013, 1833 (12): : 2911 - 2921
  • [32] MITOTIC PERTURBATION AND G2 CELL CHROMATID ABERRATIONS .5.
    SAVAGE, JRK
    PAPWORTH, DG
    REVISTA BRASILEIRA DE GENETICA, 1994, 17 (01): : 121 - 125
  • [33] COMPARATIVE-STUDY OF RADIATION-INDUCED G2 PHASE DELAY AND CHROMATID DAMAGE IN FAMILIES WITH ATAXIA-TELANGIECTASIA
    CHEN, P
    FARRELL, A
    HOBSON, K
    GIRJES, A
    LAVIN, M
    CANCER GENETICS AND CYTOGENETICS, 1994, 76 (01) : 43 - 46
  • [34] THE INFLUENCE OF CELL-KINETICS AND RADIATION-DOSE ON THE RADIATION-INDUCED BLOCK OF CELLS IN G2
    RUTGERS, DH
    VANOOSTRUM, IEA
    VANDERDUSSEN, MFN
    WILS, IS
    HEESTERS, MAAM
    TERHAARD, CHJ
    INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, 1989, 55 (06) : 1045 - 1045
  • [35] Early and late G(2) arrest of cells undergoing radiation-induced apoptosis or micronucleation
    Abend, M
    Gilbertz, KP
    Rhein, A
    vanBeuningen, D
    CELL PROLIFERATION, 1996, 29 (02) : 101 - 113
  • [36] p53 regulates Cdc2 independently of inhibitory phosphorylation to reinforce radiation-induced G2 arrest in human cells
    Winters, ZE
    Ongkeko, WM
    Harris, AL
    Norbury, CJ
    ONCOGENE, 1998, 17 (06) : 673 - 684
  • [37] p53 regulates Cdc2 independently of inhibitory phosphorylation to reinforce radiation-induced G2 arrest in human cells
    Z E Winters
    W M Ongkeko
    A L Harris
    C J Norbury
    Oncogene, 1998, 17 : 673 - 684
  • [38] P34Cdc2 kinase activity is excluded from the nucleus during the radiation-induced G2 arrest in HeLa cells
    Kao, GD
    McKenna, WG
    Muschel, RJ
    JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (49) : 34779 - 34784
  • [39] NUMERICAL RELATIONSHIP BETWEEN CELLS WITH RADIATION-INDUCED CHROMOSOME-ABERRATIONS AND CELLS LETHALLY INJURED BY RADIATION
    VIRSIK, RP
    HARDER, D
    RADIATION AND ENVIRONMENTAL BIOPHYSICS, 1980, 18 (01) : 73 - 77