Reference

Effect of 5-bromodeoxyuridine substitution on sister chromatid exchange induction by chemicals

Effect of 5-bromodeoxyuridine substitution on sister chromatid exchange induction by chemicals. Morgan, William F.; Wolff, Sheldon (Lab. Radiobiol. Environ. Health, Univ. California, San Francisco, CA 94143, USA). Chromosoma, 89(4), 285-9 (English) 1984. CODEN: CHROAU. ISSN: 0009-5915. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The effect of 5-bromodeoxyuridine (BrdU)(I) [59-14-3] incorporation on sister chromatid exchange (SCE) induction by labeling cells with BrdU for the 1st cell cycle or the 1st and 2nd cell cycles was investigated. The cells were then treated with bleomycin [11056-06-7], which produces DNA strand breakage; proflavine [92-62-6], which intercalates into DNA; mitomycin C [50-07-7], which produces monoadducts and DNA crosslinks; or aphidicolin [38966-21-1], which inhibits DNA polymerase a. The chems. were added before BrdU exposure or during the 1st, 2nd, or both cell cycles. Only mitomycin C, which induces long-lived lesions, elevated the SCE frequency when cells were treated before BrdU labeling. When bleomycin, proflavine, or mitomycin C was present concurrently with BrdU, the frequency of SCEs was increased independently of the BrdU labeling protocol. Aphidicolin, on the other hand, induced more SCEs when present for the 2nd cell cycle, when DNA replicates on a template DNA strand contg. BrdU. The induction of SCEs in the 1st cell cycle (twins) and in the 2nd cell cycle (singles) after continuous treatment of the cells with BrdU and the test chems. was also examd. Only aphidicolin increased SCE frequency in the 2nd cell cycle. Thus, aphidicolin, but not bleomycin, proflavine, or mitomycin C, affects BrdU-substituted DNA and unsubstituted DNA differently. This type of interaction should be taken into consideration when the SCE test is used as an assay system.

Aphidicolin and deoxycoformycin cause DNA breaks and cell death in unstimulated human lymphocytes

Aphidicolin and deoxycoformycin cause DNA breaks and cell death in unstimulated human lymphocytes. Brox, L.; Hunting, D.; Belch, A. (Cross Cancer Inst., Univ. Alberta, Edmonton, AB T6G 2H7, Can.). Biochem. Biophys. Res. Commun., 120(3), 959-63 (English) 1984. CODEN: BBRCA9. ISSN: 0006-291X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Human lymphocytes lose viability when incubated in vitro with either aphidicolin [38966-21-1], an inhibitor of DNA polymerase a, or with the combination of aphidicolin and deoxycoformycin [53910-25-1] (an adenosine deaminase inhibitor). The loss of viability was rapid with the combination of aphidicolin (2 mg/mL) and deoxycoformycin (1 mg/mL) with essentially complete loss of viability after 72 h of incubation. This drug combination produces DNA single-strand breaks after 24 and 48 h of incubation at a level equiv. to that produced by 200 or 400R of x-irradn., resp.