An investigation using inhibition of G2 repair of the molecular basis of lesions which result in chromosomal aberrations.

Abstract

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.

• Authors: R C Moore, C Randell, M A Bender
• Journal: Mutation research (Mutat Res) Vol. 199 Issue 1 Pg. 229-33 (May 1988) ISSN: 0027-5107 [Print] Netherlands
• PMID: 3129653 (Publication Type: Journal Article)

Chemical References

• Diterpenes
• Cytarabine
• Aphidicolin

Topics

• Animals
• Aphidicolin
• Cells, Cultured
• Chromosome Aberrations
• Cytarabine (pharmacology)
• DNA Damage
• DNA Repair (drug effects)
• Diterpenes (pharmacology)
• Interphase
• Sister Chromatid Exchange (drug effects)
• X-Rays