|| Checking for direct PDF access through Ovid
It is generally believed that the mammalian nucleotide excision repair pathway removes DNA helix-distorting bulky DNA lesions, while small non-bulky lesions are repaired by base excision repair (BER). However, recent work demonstrates that the oxidativly generated guanine oxidation products, spiroimininodihydantoin (Sp), 5-guanidinohydantoin (Gh), and certain intrastrand cross-linked lesions, are good substrates of NER and BER pathways that compete with one another in human cell extracts. The oxidation of guanine by peroxynitrite is known to generate 5-guanidino-4-nitroimidazole (NIm) which is structurally similar to Gh, except that the 4-nitro group in NIm is replaced by a keto group in Gh. However, unlike Gh, NIm is an excellent substrate of BER, but not of NER. These and other related results are reviewed and discussed in this article.Non-bulky guanine lesions are removed by Nucleotide Excision Repair mechanisms.DNA Intrastrand cross-linked G[C8-N3]T-thymine lesions are substrates of BER and NER.DNA hydantoin lesions are repaired by competitive BER and NER pathways.The DNA guanine lesion 5-guanidino-4-nitroimidazole is repaired by BER but not NER.