Complementation of the oxidatively damaged DNA repair defect in Cockayne syndrome A and B cells by Escherichia coli formamidopyrimidine DNA glycosylase.
Free Radic Biol Med
; 42(12): 1807-17, 2007 Jun 15.
Article
en En
| MEDLINE
| ID: mdl-17512460
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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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Daño del ADN
/
Síndrome de Cockayne
/
ADN-Formamidopirimidina Glicosilasa
/
Reparación del ADN
/
Escherichia coli
/
Prueba de Complementación Genética
Límite:
Adolescent
/
Adult
/
Aged
/
Aged80
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
Free Radic Biol Med
Asunto de la revista:
BIOQUIMICA
/
MEDICINA
Año:
2007
Tipo del documento:
Article
País de afiliación:
Italia