Abstract |
Repair of the oxidized purine 8-oxo-7,8-dihydroguanine (8-oxoGua) is inefficient in cells belonging to the B complementation group of Cockayne syndrome (CS-B), a developmental and neurological disorder characterized by defective transcription-coupled repair. We show here that cells belonging to the A complementation group (CS-A) are also defective in repair of 8-oxoGua and we demonstrate that expression of the Escherichia coli formamidopyrimidine DNA glycosylase (FPG) completely corrects the repair deficiency in both CS-A and CS-B cells. Phenotypically, CS-A cells are normally sensitive to toxicity and micronuclei induced by the oxidizing agent potassium bromate. CS-B cells display sensitivity to elevated concentrations of potassium bromate but this is not compensated by FPG expression, suggesting toxicity of lesions that are not FPG substrates. The data indicate that 8-oxoGua is not a major toxic and clastogenic lesion in CS cells.
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Authors | Monica Ropolo, Paolo Degan, Mara Foresta, Mariarosaria D'Errico, Denise Lasigliè, Eugenia Dogliotti, Gianluigi Casartelli, Simonetta Zupo, Alessandro Poggi, Guido Frosina |
Journal | Free radical biology & medicine
(Free Radic Biol Med)
Vol. 42
Issue 12
Pg. 1807-17
(Jun 15 2007)
ISSN: 0891-5849 [Print] United States |
PMID | 17512460
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Bromates
- Carcinogens
- potassium bromate
- DNA-Formamidopyrimidine Glycosylase
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Topics |
- Adolescent
- Adult
- Aged
- Aged, 80 and over
- Bromates
(pharmacology)
- Carcinogens
(pharmacology)
- Cell Survival
(drug effects)
- Cells, Cultured
(drug effects)
- Cockayne Syndrome
(genetics)
- Colony-Forming Units Assay
- DNA Damage
- DNA Repair
- DNA-Formamidopyrimidine Glycosylase
(genetics, metabolism)
- Escherichia coli
(enzymology)
- Female
- Fibroblasts
(drug effects)
- Genetic Complementation Test
- Genetic Vectors
- Humans
- Kidney
(metabolism, pathology)
- Male
- Micronucleus Tests
- Transcription, Genetic
- Urinary Bladder Neoplasms
(metabolism, pathology)
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