Mutagenicity of secondary oxidation products of 8-oxo-7,8-dihydro-2′-deoxyguanosine 5′-triphosphate (8-hydroxy-2′- deoxyguanosine 5′-triphosphate)

Hori, Mika; Suzuki, Tetsuya; Minakawa, Noriaki; Matsuda, Akira; Harashima, Hideyoshi; Kamiya, Hiroyuki

doi:10.1016/j.mrfmmm.2011.05.015

Cited by 9 publications

(12 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, many carcinogens cause adducts on guanine. Alternatively, an exposure could be endogenous in origin, for example reactive oxygen species (Hori et al., 2011) or intermediates of oxidative estrogen metabolism (Spencer et al., 2012). Both can cause damage to guanine and, although preferentially repaired by BER, some lesions can be substrates for TCR (Hanawalt and Spivak, 2008).…”

Section: Discussionmentioning

confidence: 99%

Mutational Processes Molding the Genomes of 21 Breast Cancers

Nik-Zainal

Alexandrov

Wedge

et al. 2012

Cell

1,736

1,891

View full text Add to dashboard Cite

SummaryAll cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed “kataegis,” was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed.PaperClip

show abstract

Section: Discussionmentioning

confidence: 99%

Mutational Processes Molding the Genomes of 21 Breast Cancers

Nik-Zainal

Alexandrov

Wedge

et al. 2012

Cell

1,736

1,891

View full text Add to dashboard Cite

show abstract

“…Interestingly, in contrast to the potent mutagenicity of Gh and Sp when the lesions are replicated by polymerases in vitro and in vivo , when dGhTP and dSpTP were introduced to the nucleotide pool of wild-type E. coli , no increase in mutation frequency was observed [103]. Furthermore, MutT was not able to hydrolyze the hyperoxidized triphosphates in vitro suggesting that the absence of mutagenicity of dGhTP and dSpTP might be due to the inability of E. coli polymerases to incorporate the lesions in vivo , or that the lesions are incorporated opposite G to form the ‘correct’ base pair [103]. Further studies are needed to understand the lack of mutagenicity of hyperoxidized lesions when the lesions are part of the nucleotide pool.…”

Section: Mutational and Genotoxic Properties Of Oxidatively Damaged Dnamentioning

confidence: 99%

Chemical and biological consequences of oxidatively damaged guanine in DNA

Delaney¹,

Jarem²,

Volle³

et al. 2012

Free Radical Research

View full text Add to dashboard Cite

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.

show abstract

“…The lower redox potential of 8‐oxoG as compared to that of guanine makes it even more reactive than guanine for further modifications by ROS, RNOS, and other free radicals. One of the mutagenic products formed from the oxidation of 8‐oxoG is Sp . Sp has been reported to be more mutagenic and deleterious than 8‐oxoG and other oxidized guanine products such as guanidinohydantoin ( Gh ) and imidazolone ( Iz ) .…”

Section: Introductionmentioning

confidence: 99%

“…One of the mutagenic products formed from the oxidation of 8‐oxoG is Sp . Sp has been reported to be more mutagenic and deleterious than 8‐oxoG and other oxidized guanine products such as guanidinohydantoin ( Gh ) and imidazolone ( Iz ) . Both in vitro and in vivo experimental studies have shown that Sp can induce G → C and G → T transversion mutations .…”

Section: Introductionmentioning

confidence: 99%

Base pairing patterns of DNA base lesion spiroiminodihydantoin: A DFT study

Mishra

2013

Int. J. Quantum Chem.

View full text Add to dashboard Cite

The DNA base lesion spiroiminodihydantoin (Sp) is produced in biological systems endogenously and can cause mutation and cancer. It is considered to be more mutagenic and deleterious than 8-oxoguanine and other oxidized guanine products such as guanidinohydantoin (Gh) and imidazolone. In this work, the base pairing patterns of Sp with each of the normal nucleic acid bases of DNA have been investigated thoroughly using the B3LYP, M06-2X, and wB97X-D functionals of density functional theory in conjunction with the aug-cc-pVDZ basis set. It is found that the magnitudes of interaction energies between the bases and Sp follow the order: Sp-guanine >> Sp-cytosine > Sp-adenine > Sp-thymine. The strong Sp-guanine abnormal base pairing may be the main cause of the observed mutagenicity of Sp.

show abstract

Mutagenicity of secondary oxidation products of 8-oxo-7,8-dihydro-2′-deoxyguanosine 5′-triphosphate (8-hydroxy-2′- deoxyguanosine 5′-triphosphate)

Abstract: is oxidized more easily than normal nucleobases, which can produce spiroiminodihydantoin (Sp) and guanidinohydantoin (Gh). These secondary oxidation products of 8-oxo-7,8-dihydroguanine are highly mutagenic when formed within DNA. To

Cited by 9 publications

References 36 publications

Mutational Processes Molding the Genomes of 21 Breast Cancers

Mutational Processes Molding the Genomes of 21 Breast Cancers

Chemical and biological consequences of oxidatively damaged guanine in DNA

Base pairing patterns of DNA base lesion spiroiminodihydantoin: A DFT study

Contact Info

Product

Resources

About