Repair of Bleomycin-damaged DNA by human fibroblasts

Journal of Supramolecular Structure and Cellular Biochemistry
M M HurtR E Moses

Abstract

The ability of human fibroblasts to repair bleomycin-damaged DNA was examined in vivo. Repair of the specific lesions caused by bleomycin (BLM) was investigated in normal cell strains as well as those isolated from patients with apparent DNA repair defects. The diseases ataxia telangiectasia (AT), Bloom syndrome (BS), Cockayne syndrome (CS), Fanconi anemia (FA), and xeroderma pigmentosum (XP) were those selected for study. The method used for studying the repair of DNA after BLM exposure was alkaline sucrose gradient centrifugation. After exposure to BLM, a fall in the molecular weight of DNA was observed, and after drug removal the DNA reformed rapidly to high molecular weight. The fall in molecular weight upon exposure to BLM was observed in all cells examined with the exception of some XP strains. Prelabeled cells from some XP complementation groups were found to have a higher percentage of low molecular weight DNA on alkaline gradients than did normal cells. This prelabeled low molecular weight DNA disappeared upon exposure to BLM.

References

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Citations

Jan 1, 1983·Pharmacology & Therapeutics·P R Twentyman
Nov 1, 1983·Proceedings of the National Academy of Sciences of the United States of America·M M HurtR E Moses
Aug 30, 2005·Optometry and Vision Science : Official Publication of the American Academy of Optometry·Mark S HorswillJohn P Wann
Sep 15, 2000·Clinical Orthopaedics and Related Research·K K AnbariJ P Dormans
Apr 1, 1986·Experimental Cell Research·M M Hurt, R E Moses

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