The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Removal of oxygen free-radical-induced 5′,8-purine cyclodeoxynucleosides from DNA by the nucleotide excision-repair pathway in human cells
Open accessAbstract
Exposure of cellular DNA to reactive oxygen species generates several classes of base lesions, many of which are removed by the base excision-repair pathway. However, the lesions include purine cyclodeoxynucleoside formation by intramolecular crosslinking between the C-8 position of adenine or guanine and the 5′ position of 2-deoxyribose. This distorting form of DNA damage, in which the purine is attached by two covalent bonds to the sugar-phosphate backbone, occurs as distinct diastereoisomers. It was observed here that both diastereoisomers block primer extension by mammalian and microbial replicative DNA polymerases, using DNA with a site-specific purine cyclodeoxynucleoside residue as template, and consequently appear to be cytotoxic lesions. Plasmid DNA containing either the 5′ R or 5′ S form of 5′,8-cyclo-2-deoxyadenosine was a substrate for the human nucleotide excision-repair enzyme complex. The R diastereoisomer was more efficiently repaired than the S isomer. No correction of the lesion by direct damage reversal or base excision repair was detected. Dual incision around the lesion depended on the core nucleotide excision-repair protein XPA. In contrast to several other types of oxidative DNA damage, purine cyclodeoxynucleosides are chemically stable and would be expected to accumulate at a slow rate over many years in the DNA of nonregenerating cells from xeroderma pigmentosum patients. High levels of this form of DNA damage might explain the progressive neurodegeneration seen in XPA individuals.
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Cites
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Molecular mechanism of nucleotide excision repair
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Preferential binding of the xeroderma pigmentosum group A complementing protein to damaged DNA
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Self-citationBase Excision Repair of Oxidative DNA Damage Activated by XPG Protein
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Self-citationThe intracellular signal for induction of resistance to alkylating agents in E. coli
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Oxidative DNA damage: mechanisms, mutation, and disease
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Oxidative DNA damage and disease: induction, repair and significance
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Repair of Endogenous DNA Damage
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Self-citationOxidative damage to DNA: formation, measurement and biochemical features
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Self-citationPremature Aging in Mice Deficient in DNA Repair and Transcription
de Boer, J., Andressoo, J. O., de Wit, J., Huijmans, J., Beems, R. B., van Steeg, H., Weeda, G., van der Horst, G. T. J., van Leeuwen, W., Themmen, A. P. N., et al. (2002) · Science · doi:10.1126/science.1070174 · Cited by 545
Metadata
- Authors
- Kuraoka, I., Bender, C., Romieu, A., Cadet, J., Wood, R. D., & Lindahl, T.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2000-04-04
- Volume
- 97
- Issue
- 8
- Pages
- 3832-3837
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2113912029
- Cited by
- 351
- References
- 31
- FWCI
- 5.18
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Removal of oxygen free-radical-induced 5′,8-purine cyclodeoxynucleosides from DNA by the nucleotide excision-repair pathway in human cells. https://app.cochat.ai/papers/10.1073/pnas.070471597
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- Kuraoka, I., Bender, C., Romieu, A., Cadet, J., Wood, R. D., & Lindahl, T. (2000). Removal of oxygen free-radical-induced 5′,8-purine cyclodeoxynucleosides from DNA by the nucleotide excision-repair pathway in human cells. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.070471597
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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