Folate- and deoxyuridine-sensitive chromatid breakage may result from DNA repair during G2.
A substantial increase in chromosome breakage was seen in proliferating human lymphocytes treated with 1-beta-D-arabinofuranosyl cytosine (cytosine arabinoside, cytarabine, araC) during the last 2 h of culture. The increase was larger in low folate media than in high folate media and larger still in low folate media supplemented by deoxyuridine. Similar results were found when cells were exposed to aphidicolin for the last 2 h of culture. The results provide additional evidence that folate-sensitive chromosome breakage is a consequence of abnormal DNA synthesis (in particular incorporation of deoxyuridine) and subsequent attempts during G2 to repair the abnormal DNA.
D016590:Aphidicolin; D002869:Chromosome Aberrations; D002873:Chromosome Fragility; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair; D003857:Deoxyuridine / Q000494:pharmacology*; D004224:Diterpenes / Q000494:pharmacology; D005492:Folic Acid / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007399:Interphase; D008214:Lymphocytes / Q000502:physiology; D014498:Uracil / Q000378:metabolism
D004224:Diterpenes; D003561:Cytarabine; D016590:Aphidicolin; D014498:Uracil; D005492:Folic Acid; D003857:Deoxyuridine