Literature DB >> 6733802

The inhibition of ultraviolet radiation-induced DNA repair in human diploid fibroblasts by arabinofuranosyl nucleosides.

R D Snyder, B van Houten, J D Regan.   

Abstract

The antiviral compounds 9-beta-D-arabinofuranosyladenine (ara-A), 9-beta-D-arabinofuranosyl-2-fluoroadenine (FAA), 9-beta-D-arabinofuranosylhypoxanthine (ara-Hx), 9-beta-D-arabinofuranosylguanine (ara-G), 1-beta-D-arabinofuranosylthymine (ara-T), 1-beta-D-arabinofuranosyl-2'-fluorocytosine (FAC), 1-beta-D-arabinofuranosyl-2'-fluoro-5-iodocytosine (FIAC) and 1-beta-D-arabinofuranosyl-2'-fluoro-5-methyluracil (FMAU) were compared to 1-beta-D-arabinofuranosyl cytosine (ara-C) in their ability to inhibit ultraviolet (UV) light-induced DNA repair in log phase and confluent human diploid fibroblasts. Inhibition of the polymerization or ligation steps of DNA excision repair manifests itself in the form of DNA single-strand breaks which may be quantitated through velocity sedimentation analysis in alkaline sucrose gradients. In UV-irradiated quiescent, confluent human fibroblast cultures, treatment with any of the aranucleosides leads to accumulation of single-strand breaks but the effective dose for this inhibition varies greatly. The order of their effectiveness in confluent cultures was ara-C and its derivatives greater than ara-A, FAA, ara-G, ara-Hx greater than ara-T. In rapidly cycling cells on the other hand, sensitivity to repair inhibition was exhibited only in response to ara-C and FAC. If 2 mM hydroxyurea (HU) was administered with ara-A, FAA or FMAU, however, DNA strand breaks were seen. HU also increased the efficiencies of ara-C and FAC. No significant strand breaks were observed in UV-irradiated log phase cells treated with FIAC, ara-Hx, ara-G or ara-T even in the presence of HU. The efficiencies of inhibition of unscheduled DNA synthesis (UDS) and semiconservative DNA synthesis by the aranucleosides is consistent with their relative efficiencies at producing strand breaks. The ability of the aranucleosides to inhibit DNA repair is discussed with respect to their hypothesized effects on DNA metabolic processes in eucaryotic cells.

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Year:  1984        PMID: 6733802     DOI: 10.1016/0009-2797(84)90127-3

Source DB:  PubMed          Journal:  Chem Biol Interact        ISSN: 0009-2797            Impact factor:   5.192


  4 in total

1.  Genetic complementation of UV-induced DNA repair in Chinese hamster ovary cells by the denV gene of phage T4.

Authors:  K Valerie; J K de Riel; E E Henderson
Journal:  Proc Natl Acad Sci U S A       Date:  1985-11       Impact factor: 11.205

Review 2.  DNA damage response in peripheral nervous system: coping with cancer therapy-induced DNA lesions.

Authors:  Ella W Englander
Journal:  DNA Repair (Amst)       Date:  2013-05-16

3.  Neurotoxicity of cytarabine (Ara-C) in dorsal root ganglion neurons originates from impediment of mtDNA synthesis and compromise of mitochondrial function.

Authors:  Ming Zhuo; Murat F Gorgun; Ella W Englander
Journal:  Free Radic Biol Med       Date:  2018-04-23       Impact factor: 7.376

4.  Inhibitors of ribonucleotide reductase alter DNA repair in human fibroblasts through specific depletion of purine deoxynucleotide triphosphates.

Authors:  R D Snyder
Journal:  Cell Biol Toxicol       Date:  1984-10       Impact factor: 6.691

  4 in total

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