Chemical and biological consequences of oxidatively damaged guanine in DNA - PubMed
Review
Chemical and biological consequences of oxidatively damaged guanine in DNA
Sarah Delaney et al. Free Radic Res. 2012 Apr.
Abstract
Of the four native nucleosides, 2'-deoxyguanosine (dGuo) is most easily oxidized. Two lesions derived from dGuo are 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (Fapy)∙dGuo. Furthermore, while steady-state levels of 8-oxodGuo can be detected in genomic DNA, it is also known that 8-oxodGuo is more easily oxidized than dGuo. Thus, 8-oxodGuo is susceptible to further oxidation to form several hyperoxidized dGuo products. This review addresses the structural impact, the mutagenic and genotoxic potential, and biological implications of oxidatively damaged DNA, in particular 8-oxodGuo, Fapy∙dGuo, and the hyperoxidized dGuo products.
Figures

Structure of (A) 8-oxoG and (B) Fapy·G.

Formation of 8-oxoG and Fapy·G from a common precursor.

Summary of the 8-oxoG-derived hyperoxidized G products.

Structure of (A) 8-oxoG(anti):C(anti) and (B) 8-oxoG(syn):A(anti) base pair.

Structure of (A) α-Fapy·G and (B) β-Fapy·G.

Structure of Fapy·G(syn):A(anti) base pair with two rotamers of the formamide group of Fapy·G shown (top and bottom).

Toxic oxidation cycle. (1) Genomic DNA is oxidized to generate 8-oxoG and (2) OGG1 and APE1 initiate BER by removing the oxidatively damaged nucleobase from duplex TNR DNA (shown as dotted lines) and cleaving the backbone at the abasic site. (3) The resulting gap is repaired via LP-BER, producing a TNR flap that (4) is refractory to FEN1 and ligation occurs, trapping a stem-loop hairpin in the duplex. (5) The resulting stem-loop hairpin is highly susceptible to DNA damage in the loop region and the lack of efficient repair of this damage by OGG1 results in (6) its being incorporated into the expanded duplex. The final product of the cycle now contains DNA damage that will be recognized by OGG1. Therefore, the cycle is repeated and the DNA can be processed again, incrementally expanding the TNR tract of DNA.
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