Enhancement of DNA repair capacity of mammalian cells by carcinogen treatment
To determine whether DNA excision repair is enhanced in mammalian cells in response to DNA damage, as it is in bacteria as part of the SOS response, we used an expression vector-host cell reactivation assay to measure cellular DNA repair capacity. When UV-damaged chloramphenicol acetyltransferase (CAT) vector DNA was introduced into monkey cells (CV-1), the level of CAT activity was inversely related to the UV fluence due to inhibition of CAT gene expression by UV photoproducts. When CV-1 cells were treated with either UV radiation or mitomycin C, 24-48 h before transfection, CAT expression from the UV-irradiated plasmid was increased. This increase also occurred in a line of normal human cells, but not in repair-deficient human xeroderma pigmentosum cells. We confirmed that this increase in CAT expression was due to repair, and not to production of damage-free templates by recombination; the frequency of generation of supF+ recombinants after transfection with UV-irradiated pZ189 vectors carrying different point mutations in the supF gene did not significantly increase in carcinogen-treated CV-1 cells. From these results we conclude that carcinogen treatment enhances the excision-repair capacity of normal mammalian cells.
- Research Organization:
- National Institute of Child Health and Human Development, Bethesda, MD (USA)
- OSTI ID:
- 7071900
- Journal Information:
- Somatic Cell Mol. Gen.; (United States), Journal Name: Somatic Cell Mol. Gen.; (United States) Vol. 14:4; ISSN SCMGD
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
Cells
& Tissue Culture
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL CELLS
ANIMALS
ANTI-INFECTIVE AGENTS
ANTIBIOTICS
ANTIMITOTIC DRUGS
ANTINEOPLASTIC DRUGS
BIOLOGICAL RECOVERY
BIOLOGICAL REPAIR
CARCINOGENS
DNA
DNA REPAIR
DRUGS
ELECTROMAGNETIC RADIATION
ENZYME ACTIVITY
ENZYMES
GENE RECOMBINATION
MAMMALS
MITOMYCIN
MONKEYS
MUTATIONS
NUCLEIC ACIDS
ORGANIC COMPOUNDS
PRIMATES
RADIATIONS
RADIOSENSITIVITY EFFECTS
RECOMBINANT DNA
RECOVERY
REPAIR
TRANSFERASES
ULTRAVIOLET RADIATION
VERTEBRATES
XP CELLS