Clustered DNA Damage: Electronic Properties and Their Influence on Charge Transfer. 7,8-Dihydro-8-Oxo-2'-Deoxyguaosine Versus 5',8-Cyclo-2'-Deoxyadenosines: A Theoretical Approach.
Identifieur interne : 000156 ( Main/Exploration ); précédent : 000155; suivant : 000157Clustered DNA Damage: Electronic Properties and Their Influence on Charge Transfer. 7,8-Dihydro-8-Oxo-2'-Deoxyguaosine Versus 5',8-Cyclo-2'-Deoxyadenosines: A Theoretical Approach.
Auteurs : Boleslaw T. Karwowski [Pologne]Source :
- Cells [ 2073-4409 ] ; 2020.
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.
DOI: 10.3390/cells9020424
PubMed: 32059490
PubMed Central: PMC7072346
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Muszynskiego 1, 90-151 Lodz</wicri:regionArea><wicri:noRegion>90-151 Lodz</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32059490</idno><idno type="pmid">32059490</idno><idno type="doi">10.3390/cells9020424</idno><idno type="pmc">PMC7072346</idno><idno type="wicri:Area/Main/Corpus">000148</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000148</idno><idno type="wicri:Area/Main/Curation">000148</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000148</idno><idno type="wicri:Area/Main/Exploration">000148</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Clustered DNA Damage: Electronic Properties and Their Influence on Charge Transfer. 7,8-Dihydro-8-Oxo-2'-Deoxyguaosine Versus 5',8-Cyclo-2'-Deoxyadenosines: A Theoretical Approach.</title><author><name sortKey="Karwowski, Boleslaw T" sort="Karwowski, Boleslaw T" uniqKey="Karwowski B" first="Boleslaw T" last="Karwowski">Boleslaw T. Karwowski</name><affiliation wicri:level="1"><nlm:affiliation>DNA Damage Laboratory of Food Science Department, Faculty of Pharmacy, Medical University of Lodz, ul. Muszynskiego 1, 90-151 Lodz, Poland.</nlm:affiliation><country xml:lang="fr">Pologne</country><wicri:regionArea>DNA Damage Laboratory of Food Science Department, Faculty of Pharmacy, Medical University of Lodz, ul. Muszynskiego 1, 90-151 Lodz</wicri:regionArea><wicri:noRegion>90-151 Lodz</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cells</title><idno type="eISSN">2073-4409</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Approximately 3 × 10<sup>17</sup> 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 - <sup>oxo</sup>dG). Here, the influence of cdA, "the simplest tandem lesion", on the charge transfer through <i>ds</i>-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'<i>S</i>)- or (5'<i>R</i>)-cdA leads to a slowdown in the hole transfer by one order of magnitude between the neighboring dG<sup>oxo</sup>dG in comparison to "native" <i>ds</i>-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, <sup>oxo</sup>dG: 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.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32059490</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>24</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2073-4409</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>02</Month><Day>12</Day></PubDate></JournalIssue><Title>Cells</Title><ISOAbbreviation>Cells</ISOAbbreviation></Journal><ArticleTitle>Clustered DNA Damage: Electronic Properties and Their Influence on Charge Transfer. 7,8-Dihydro-8-Oxo-2'-Deoxyguaosine Versus 5',8-Cyclo-2'-Deoxyadenosines: A Theoretical Approach.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E424</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/cells9020424</ELocationID><Abstract><AbstractText>Approximately 3 × 10<sup>17</sup> 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 - <sup>oxo</sup>dG). Here, the influence of cdA, "the simplest tandem lesion", on the charge transfer through <i>ds</i>-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'<i>S</i>)- or (5'<i>R</i>)-cdA leads to a slowdown in the hole transfer by one order of magnitude between the neighboring dG<sup>oxo</sup>dG in comparison to "native" <i>ds</i>-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, <sup>oxo</sup>dG: 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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Karwowski</LastName><ForeName>Boleslaw T</ForeName><Initials>BT</Initials><AffiliationInfo><Affiliation>DNA Damage Laboratory of Food Science Department, Faculty of Pharmacy, Medical University of Lodz, ul. Muszynskiego 1, 90-151 Lodz, Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>02</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cells</MedlineTA><NlmUniqueID>101600052</NlmUniqueID><ISSNLinking>2073-4409</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">5′,8-cyclo-2′-deoxyadenosines</Keyword><Keyword MajorTopicYN="Y">Base Excision Repair</Keyword><Keyword MajorTopicYN="Y">Charge transfer</Keyword><Keyword MajorTopicYN="Y">Clustered DNA damage</Keyword><Keyword MajorTopicYN="Y">DFT</Keyword><Keyword MajorTopicYN="Y">Glycosylases</Keyword></KeywordList><CoiStatement>The author 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