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Even though epidemiological studies have identified arsenic compounds as carcinogenic to humans, they are not mutagenic in bacterial and mammalian test systems. However, they increase the mutagenicity and clastogenicity in combination with other DNA damaging agents and there are indications of inhibition of DNA repair processes. We investigated the effect(More)
Nucleotide excision repair (NER) mechanism is the major pathway responsible for the removal of a large variety of bulky lesions from the genome. Two different NER subpathways have been identified, i.e. the transcription-coupled and the global genome repair pathways. For DNA-damage induced by ultraviolet light both transcription-coupled repair and global(More)
We compared the susceptibilities of cultured melanocytes and keratinocytes to dimer induction in DNA by monochromatic ultraviolet (UV) radiation. Keratinocytes as well as melanocytes were derived from human foreskin, grown as a monolayer in petri dishes, covered with phosphate-buffered saline containing 0.1% glucose, and irradiated. UV irradiation was(More)
Two of the hallmarks of Cockayne's syndrome (CS) are the hypersensitivity of cells to UV light and the lack of recovery of the ability to synthesize RNA following exposure of cells to UV light, in spite of the normal repair capacity at the overall genome level. The prolonged repressed RNA synthesis has been attributed to a defect in transcription-coupled(More)
Host-cell reactivation (HCR) of UV-C-irradiated herpes simplex virus type 1 (HSV-1) has been determined in skin fibroblasts from the following hereditary cancer-prone syndromes: aniridia (AN), dysplastic nevus syndrome (DNS), Von Hippel-Lindau syndrome (VHL), Li-Fraumeni syndrome (LFS) and a family with high incidence of breast and ovarian cancer. Cells(More)
The N-(deoxyguanosine-8-yl)-2-acetylaminofluorene (dG-C8-AAF) lesion is among the most helix distorting DNA lesions. In normal fibroblasts dG-C8-AAF is repaired rapidly in transcriptionally active genes, but without strand specificity, indicating that repair of dG-C8-AAF by global genome repair (GGR) overrules transcription-coupled repair (TCR). Yet,(More)
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