TY - JOUR
T1 - Activity of nucleotide excision repair enzymes for oxanine cross-link lesions.
AU - Nakano, Toshiaki
AU - Katafuchi, Atsushi
AU - Terato, Hiroaki
AU - Suzuki, Toshinori
AU - Van Houten, Bennett
AU - Ide, Hiroshi
N1 - Copyright:
This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine
PY - 2005
Y1 - 2005
N2 - Nitric oxide and nitrous acid induce deamination of DNA bases, resulting in uracil, hypoxanthine, xanthine, and oxanine (Oxa) as major damage. Oxa reacts further with polyamines and DNA binding proteins, generating bulky cross-link adducts. Recently we have shown Oxa and cross-link adducts are potentially genotoxic lesions. In the present study, we have assessed the role of base excision repair (BER) and nucleotide excision repair (NER) systems in the repair of Oxa and Oxa-spermine (Oxa-Sp) cross-link adducts. Oxa was very poorly removed from DNA by both BER glycosylases and NER enzymes, whereas Oxa-Sp was efficiently excised by E. coli and human NER enzymes.
AB - Nitric oxide and nitrous acid induce deamination of DNA bases, resulting in uracil, hypoxanthine, xanthine, and oxanine (Oxa) as major damage. Oxa reacts further with polyamines and DNA binding proteins, generating bulky cross-link adducts. Recently we have shown Oxa and cross-link adducts are potentially genotoxic lesions. In the present study, we have assessed the role of base excision repair (BER) and nucleotide excision repair (NER) systems in the repair of Oxa and Oxa-spermine (Oxa-Sp) cross-link adducts. Oxa was very poorly removed from DNA by both BER glycosylases and NER enzymes, whereas Oxa-Sp was efficiently excised by E. coli and human NER enzymes.
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U2 - 10.1093/nass/49.1.293
DO - 10.1093/nass/49.1.293
M3 - Article
C2 - 17150749
AN - SCOPUS:39049190805
SN - 1746-8272
SP - 293
EP - 294
JO - Nucleic acids symposium series (2004)
JF - Nucleic acids symposium series (2004)
IS - 49
ER -