{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T22:27:03Z","timestamp":1790980023284,"version":"4.1.0"},"reference-count":33,"publisher":"National Academy of Sciences","issue":"8","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2000,4,11]]},"abstract":"<jats:p>\n                    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\u2032 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\u2032\n                    <jats:italic>R<\/jats:italic>\n                    or 5\u2032\n                    <jats:italic>S<\/jats:italic>\n                    form of 5\u2032,8-cyclo-2-deoxyadenosine was a substrate for the human nucleotide excision-repair enzyme complex. The\n                    <jats:italic>R<\/jats:italic>\n                    diastereoisomer was more efficiently repaired than the\n                    <jats:italic>S<\/jats:italic>\n                    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.\n                  <\/jats:p>","DOI":"10.1073\/pnas.070471597","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:38:21Z","timestamp":1027679901000},"page":"3832-3837","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":312,"title":["Removal of oxygen free-radical-induced 5\u2032,8-purine cyclodeoxynucleosides from DNA by the nucleotide excision-repair pathway in human cells"],"prefix":"10.1073","volume":"97","author":[{"given":"Isao","family":"Kuraoka","sequence":"first","affiliation":[{"name":"Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, Hertfordshire EN6 3LD, United Kingdom; and Laboratoire des L\u00e9sions des Acides Nucl\u00e9iques, Service de Chimie Inorganique et Biologique, D\u00e9partement de Recherche Fondamentale sur la Mati\u00e8re Condens\u00e9e, 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