An investigation using inhibition of G2 repair of the molecular basis of lesions which result in chromosomal aberrations.
Cultures of JU56 cells were irradiated with 2.5 Gy X-rays and 16 h later the cultures were exposed to a moderately inhibitory dose of 1-beta-D-arabinofuranosylcytosine (ara-C) or aphidicolin (APC) and to colcemid, for 2 h. The c-metaphases collected for examination had therefore been exposed to X-rays in G1 or early S, and to the repair inhibitors APC and ara-C during the latter half of G2. It was found that treatment of cells irradiated early in cell cycle, that is, in G1 and early S, with APC or ara-C in G2, (1) reduced the frequency of chromatid and chromosome exchanges below that of cells treated with X-rays alone, (2) produced no more chromatid breaks and gaps than were seen in unirradiated cells, (3) increased the number of chromosome fragments and gaps in a more than additive fashion, and (4) produced only an additive effect, by comparison with the effect of X-rays and drug given separately, on the total number of chromosomal aberrations.
D000818:Animals; D016590:Aphidicolin; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D003561:Cytarabine / Q000494:pharmacology*; D004249:DNA Damage; D004260:DNA Repair / Q000187:drug effects*; D004224:Diterpenes / Q000494:pharmacology*; D007399:Interphase; D012854:Sister Chromatid Exchange / Q000187:drug effects; D014965:X-Rays
D004224:Diterpenes; D003561:Cytarabine; D016590:Aphidicolin