Formation of chromatid-type aberrations in G2 stage of the cell cycle.
CHO cells were treated in G1 stage of the cell cycle with chromosome-breaking agents that act in an S-dependent manner. The cells were challenged in G2 stage, before fixation, with various inhibitors of DNA synthesis or repair. Short-wave UV, mitomycin C, decarbomyl mitomycin and 4-nitroquinoline oxide (4NQO) were used as chromosome-breaking agents. The inhibitors of DNA repair or synthesis used were hydroxyurea, aphidicolin and caffeine. Permeabilization of cells followed by a treatment with Neurospora endonuclease (a treatment to convert DNA single-strand breaks into double-strand breaks) did not have any influence on the frequencies of chromatid aberrations induced by the chemicals used, whereas with the inhibitors the extent of potentiation varied depending on the mutagen and the inhibitor used.
D000818:Animals; D002460:Cell Line; D002842:Chromatids / Q000032:analysis*; D002869:Chromosome Aberrations; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair / Q000187:drug effects; D004261:DNA Replication / Q000187:drug effects / Q000528:radiation effects; D005260:Female; D007399:Interphase; D009153:Mutagens / Q000494:pharmacology; D010053:Ovary / Q000166:cytology
D009153:Mutagens