Abstract：
:Approximately 3 × 1017 DNA damage events take place per hour in the human body. Within clustered DNA lesions, they pose a serious problem for repair proteins, especially for iron-sulfur glycosylases (MutyH), which can recognize them by the electron-transfer process. It has been found that the presence of both 5',8-cyclo-2'-deoxyadenosine (cdA) diastereomers in the ds-DNA structure, as part of a clustered lesion, can influence vertical radical cation distribution within the proximal part of the double helix, i.e., d[~oxoGcAoxoG~] (7,8-dihydro-8-oxo-2'-deoxyguaosine - oxodG). Here, the influence of cdA, "the simplest tandem lesion", on the charge transfer through ds-DNA was taken into theoretical consideration at the M062x/6-31+G** level of theory in the aqueous phase. It was shown that the presence of (5'S)- or (5'R)-cdA leads to a slowdown in the hole transfer by one order of magnitude between the neighboring dGoxodG in comparison to "native" ds-DNA. Therefore, it can be concluded that such clustered lesions can lead to defective damage recognition with a subsequent slowing down of the DNA repair process, giving rise to an increase in mutations. As a result, the unrepaired, oxodG: dA base pair prior to genetic information replication can finally result in GC TA or ATCG transversion. This type of mutation is commonly observed in human cancer cells. Moreover, because local multiple damage sites (LMSD) are effectively produced as a result of ionization factors, the presented data in this article might be useful in developing a new scheme of radiotherapy treatment against the background of DNA repair efficiency.
journal_name
Cellsjournal_title
Cellsauthors
Karwowski BTdoi
10.3390/cells9020424subject
Has Abstractpub_date
2020-02-12 00:00:00issue
2issn
2073-4409pii
cells9020424journal_volume
9pub_type
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