G2 chromatid aberrations: Kinetics and possible mechanisms

Journal Article · Fri Jan 01 00:00:00 EST 1993 · Environmental and Molecular Mutagenesis; (United States)

DOI:https://doi.org/10.1002/em.2850220412· OSTI ID:7199204

Bryant, P E; Slijepcevic, P ^[1]

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1. Univ. of St. Andrews (United Kingdom)

Chromatid breaks and exchanges are induced by radiation in G2 mammalian cells. Breaks are at a maximum number at about 30 min after irradiation and decrease apparently exponentially with time between irradiation and sampling. Few breaks are observed immediately following exposure, probably as a result of selection of mitotic cells where chromosomes are condensed and there is consequently a lack of time for expression of damage. The change in frequency of breaks with time, from 30 min after radiation exposure and onwards, can be interpreted in two possible ways: either in terms of a repair process or in terms of a change in radiosensitivity through G2. However, the results with an inhibitor of repair of DNA double-strand breaks (ara A) and with [open quotes]transient hypothermia[close quotes] which extends the G2 phase, argue for an interpretation based on rejoining of chromatid breaks, possibly reflecting the repair of a subclass of dsb. Data from experiments with irradiated and restriction endonuclease treated radiosensitive mutant rodent lines indicate that enhanced levels of conversion of dsb into chromosomal aberrations may be largely independent of repair rates of bulk dsb. In CHO cells and in human lymphocytes exchanges initially increase rapidly with time and then remain at a constant frequency, supporting the notion of a uniform chromosomal radiosensitivity throughout most of G2 and providing further evidence that the mechanism for misjoining broken chromatids (leading to exchanges) is different from that for rejoining of chromatid breaks. Ratios of breaks to exchanges were found to vary in different cell lines and at different times during treatment with inhibitors or at altered temperatures, possibly (in different cell lines) indicating different levels of enzymes involved in misjoining, but suggesting that the mechanisms of chromosomal rejoining and misjoining are independent, at least to some degree. 19 refs., 11 figs., 1 tab.

• OSTI ID: 7199204
• Journal Information: Environmental and Molecular Mutagenesis; (United States), Vol. 22:4; ISSN 0893-6692
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
59 BASIC BIOLOGICAL SCIENCES
CHROMOSOMAL ABERRATIONS
PRODUCTION
CHROMOSOMES
PHYSICAL RADIATION EFFECTS
STRAND BREAKS
REPAIR
CELL CYCLE
GENETIC RADIATION EFFECTS
TIME DEPENDENCE
BIOLOGICAL EFFECTS
BIOLOGICAL RADIATION EFFECTS
GENETIC EFFECTS
MUTATIONS
RADIATION EFFECTS
560120* - Radiation Effects on Biochemicals
Cells
& Tissue Culture
550200 - Biochemistry
550400 - Genetics