potassium-bromate has been researched along with Cockayne-Syndrome* in 2 studies
2 other study(ies) available for potassium-bromate and Cockayne-Syndrome
| Article | Year |
|---|---|
Complementation of the oxidatively damaged DNA repair defect in Cockayne syndrome A and B cells by Escherichia coli formamidopyrimidine DNA glycosylase.
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. Topics: Adolescent; Adult; Aged; Aged, 80 and over; Bromates; Carcinogens; Cell Survival; Cells, Cultured; Cockayne Syndrome; Colony-Forming Units Assay; DNA Damage; DNA Repair; DNA-Formamidopyrimidine Glycosylase; Escherichia coli; Female; Fibroblasts; Genetic Complementation Test; Genetic Vectors; Humans; Kidney; Male; Micronucleus Tests; Transcription, Genetic; Urinary Bladder Neoplasms | 2007 |
Potassium bromate but not X-rays cause unexpectedly elevated levels of DNA breakage similar to those induced by ultraviolet light in Cockayne syndrome (CS-B) fibroblasts.
It has been previously reported that the elevated accumulation of repair incision intermediates in cells from patients with combined characteristics of xeroderma pigmentosum complementation group D (XP-D) and Cockayne syndrome (CS) XP-D/CS fibroblasts following UV irradiation is caused by an "uncontrolled" incision of undamaged genomic DNA induced by UV-DNA-lesions which apparently are not removed. This could be an explanation for the extreme sensitivity of these cells to UV light. In the present study, we confirm the immediate DNA breakage following UV irradiation also for CS group B (CS-B) fibroblasts by DNA migration in the "comet assay" and extend these findings to other lesions such as 8-oxodeoxyguanosine (8-oxodG), selectively induced by KBrO3 treatment. In contrast, X-ray exposure does not induce differential DNA breakage. This indicates that additional lesions other than the UV-induced photoproducts (cyclobutane pyrimidine dimers, CPD, and 6-pyrimidine-4-pyrimidone products, 6-4 PP), such as 8-oxodG, specifically induced by KBrO3, are likely to trigger "uncontrolled" DNA breakage in the undamaged genomic DNA in the CS-B fibroblasts, thus accounting for some of the clinical features of these patients. Topics: Bromates; Chromosomal Instability; Cockayne Syndrome; Comet Assay; DNA; DNA Damage; DNA Repair; Fibroblasts; Guanine; Humans; Oxidation-Reduction; Photochemistry; Pyrimidine Dimers; Radiation Tolerance; Transcription, Genetic; Ultraviolet Rays; Xeroderma Pigmentosum | 2004 |