Abstract
Normal human and XP2 fibroblasts were treated with UV plus UV-mimetic chemicals. The UV dose used was sufficient to saturate the UV excision repair system. Excision repair after combined treatments was estimated by unscheduled DNA synthesis, BrdUrd photolysis, and the loss of sites sensitive to a UV specific endonuclease. Since the repair of damage from UV and its mimetics is coordinately controlled we expected that there would be similar rate-limiting steps in the repair of UV and chemical damage and that after a combined treatment the total amount of repair would be the same as from UV or the chemicals separately. The expectation was not fulfilled. In normal cells repair after a combined treatment was additive whereas in XP cells repair after a combined treatment was usually less than after either agent separately. The chemicals tested were AAAF, DMBA-epoxide, 4NQO, and ICR-170.
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Abbreviations
- AAFF:
-
N-acetoxy-acetylaminoflourene
- DMBA:
-
epoxide – 7, 12 dimethylbenz[a]anthracene 5, 6-oxide
- ICR-170:
-
Acridine mustard
- 4NQO:
-
4 nitroquinoline oxide
- XP:
-
Xeroderma pigmentosum
- UDS:
-
Unscheduled DNA synthesis
- UV:
-
Ultraviolet
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Setlow, R.B., Ahmed, F.E. (1980). DNA Repair in Human Cells Exposed to Combinations of Carcinogenic Agents. In: Pullman, B., Ts’o, P.O.P., Gelboin, H. (eds) Carcinogenesis: Fundamental Mechanisms and Environmental Effects. The Jerusalem Symposia on Quantum Chemistry and Biochemistry, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-9104-0_37
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DOI: https://doi.org/10.1007/978-94-009-9104-0_37
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