ArticleProceedings of the National Academy of Sciences of the United States of America2010
HO* radicals induce an unexpected high proportion of tandem base lesions refractory to repair by DNA glycosylases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 131 citations in OpenAlex.
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- Hole Transfer and the Resulting DNA Damage.Biomolecules · 2024Review
- Scavenging of Alkylperoxyl Radicals by Addition to Ascorbate: An Alternative Mechanism to Electron Transfer.Antioxidants (Basel, Switzerland) · 2024Article
- 8-OxodGuo and Fapy•dG Mutagenicity inChemical research in toxicology · 2024Article
- Structural Analysis and Antioxidant and Immunoregulatory Activities of an Exopolysaccharide Isolated fromMolecules (Basel, Switzerland) · 2023Article
- Hydroxyl Radical vs. One-Electron Oxidation Reactivities in an Alternating GC Double-Stranded Oligonucleotide: A New Type Electron Hole Stabilization.Biomolecules · 2023Article
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- Assessing the Formation of Purine Lesions in Mitochondrial DNA of Cockayne Syndrome Cells.Biomolecules · 2022Article
- PARP-1 Is a Potential Marker of Retinal Photooxidation and a Key Signal Regulator in Retinal Light Injury.Oxidative medicine and cellular longevity · 2022Review
- Genotoxic Mechanism of Action of TBBPA, TBBPS and Selected Bromophenols in Human Peripheral Blood Mononuclear Cells.Frontiers in immunology · 2022Article
- Hypoxia Imaging As a Guide for Hypoxia-Modulated and Hypoxia-Activated Therapy.Antioxidants & redox signaling · 2022Review
- The Two Faces of the Guanyl Radical: Molecular Context and Behavior.Molecules (Basel, Switzerland) · 2021Review
- Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease.International journal of molecular sciences · 2021Review
- Genotoxic risk assessment and mechanism of DNA damage induced by phthalates and their metabolites in human peripheral blood mononuclear cells.Scientific reports · 2021Article
- Recognition of a tandem lesion by DNA bacterial formamidopyrimidine glycosylases explored combining molecular dynamics and machine learning.Computational and structural biotechnology journal · 2021Article
- Lost in the Crowd: How Does Human 8-Oxoguanine DNA Glycosylase 1 (OGG1) Find 8-Oxoguanine in the Genome?International journal of molecular sciences · 2020Review
- UV-Induced Charge-Transfer States in Short Guanosine-Containing DNA Oligonucleotides.Chembiochem : a European journal of chemical biology · 2020Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reaction of HO(*) radicals with double-stranded calf thymus DNA produces high levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) and, to a minor extent, 8-oxo-7,8-dihydro-2'-deoxyadenosine (8-oxodAdo). Formation of the hydroxylated purine lesions is explained by addition of HO(*) to the C8 position of the purine moiety. It has been reported that tandem lesions containing a formylamine residue neighboring 8-oxodGuo could be produced through addition of a transiently generated pyrimidine peroxyl radical onto the C8 of an adjacent purine base. Formation of such tandem lesions accounted for approximately 10% of the total 8-oxodGuo. In the present work we show that addition of HO(*) onto the C8 of purine accounts for only approximately 5% of the generated 8-oxodGuo. About 50% of the 8-hydroxylated purine lesions, including 8-oxodGuo and 8-oxodAdo, are involved in tandem damage and are produced by peroxyl addition onto the C8 of a vicinal purine base. In addition, the remaining 45% of the 8-oxodGuo are produced by an electron transfer reaction, providing an explanation for the higher yield of formation of 8-oxodGuo compared to 8-oxodAdo. Interestingly, we show that >40% of the 8-oxodGuo involved in tandem lesions is refractory to excision by DNA glycosylases. Altogether our results demonstrate that, subsequently to a single oxidation event, peroxidation reactions significantly increase the yield of formation of hydroxylated purine modifications, generating a high proportion of tandem lesions partly refractory to base excision repair.
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