Excision of Oxidatively Generated Guanine Lesions by Competing Base and Nucleotide Excision Repair Mechanisms in Human Cells
The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of bo...
Saved in:
| Published in | Chemical research in toxicology Vol. 32; no. 4; pp. 753 - 761 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Chemical Society
15.04.2019
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of both base excision repair (BER) and nucleotide excision repair (NER) mechanisms in intact human cells. Site-specifically modified, 32P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells, and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2–8 h incubation periods and lysis of the cells. DNA duplexes bearing single benzo[a]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA–/– cells, while the BER yields were strongly reduced in NEIL1–/– cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil diminish the BER yields of Sp lesions and enhance the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates. |
|---|---|
| AbstractList | The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of both base excision repair (BER) and nucleotide excision repair (NER) mechanisms in intact human cells. Site-specifically modified, 32P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells, and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2–8 h incubation periods and lysis of the cells. DNA duplexes bearing single benzo[a]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA–/– cells, while the BER yields were strongly reduced in NEIL1–/– cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil diminish the BER yields of Sp lesions and enhance the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates. The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of both base excision repair (BER) and nucleotide excision repair (NER) mechanisms in intact human cells. Site-specifically modified, 32P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells, and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2-8 h incubation periods and lysis of the cells. DNA duplexes bearing single benzo[ a]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA-/- cells, while the BER yields were strongly reduced in NEIL1-/- cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil diminish the BER yields of Sp lesions and enhance the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates.The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of both base excision repair (BER) and nucleotide excision repair (NER) mechanisms in intact human cells. Site-specifically modified, 32P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells, and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2-8 h incubation periods and lysis of the cells. DNA duplexes bearing single benzo[ a]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA-/- cells, while the BER yields were strongly reduced in NEIL1-/- cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil diminish the BER yields of Sp lesions and enhance the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates. The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA, are substrates of both BER and NER mechanisms in intact human cells. Site-specifically modified, 32 P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2–8 hour incubation periods and lysis of the cells. DNA duplexes bearing single benzo[ a ]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA −/− cells, while the BER yields were strongly reduced in NEIL1 −/− cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil, diminish the BER yields of Sp lesions and enhanced the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates. The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the oxidatively generated guanine lesions spiroiminodihydantoin (Sp) and 5-guanidinohydantoin (Gh) embedded in double-stranded DNA are substrates of both base excision repair (BER) and nucleotide excision repair (NER) mechanisms in intact human cells. Site-specifically modified, P-internally labeled double-stranded DNA substrates were transfected into fibroblasts or HeLa cells, and the BER and/or NER mono- and dual incision products were quantitatively recovered after 2-8 h incubation periods and lysis of the cells. DNA duplexes bearing single benzo[ a]pyrene-derived guanine adduct were employed as positive controls of NER. The NER activities, but not the BER activities, were abolished in XPA cells, while the BER yields were strongly reduced in NEIL1 cells. Co-transfecting different concentrations of analogous DNA sequences bearing the BER substrates 5-hydroxyuracil diminish the BER yields of Sp lesions and enhance the yields of NER products. These results are consistent with a model based on the local availability of BER and NER factors in human cells and their competitive binding to the same Sp or Gh BER/NER substrates. |
| Author | Kropachev, Konstantin Kolbanovskiy, Marina Geacintov, Nicholas E Shafirovich, Vladimir |
| AuthorAffiliation | Chemistry Department |
| AuthorAffiliation_xml | – name: Chemistry Department – name: 1 Chemistry Department, New York University, 31 Washington Place, New York, NY 10003-5180, USA |
| Author_xml | – sequence: 1 givenname: Vladimir orcidid: 0000-0001-8225-6509 surname: Shafirovich fullname: Shafirovich, Vladimir email: vs5@nyu.edu – sequence: 2 givenname: Konstantin surname: Kropachev fullname: Kropachev, Konstantin – sequence: 3 givenname: Marina surname: Kolbanovskiy fullname: Kolbanovskiy, Marina – sequence: 4 givenname: Nicholas E surname: Geacintov fullname: Geacintov, Nicholas E |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30688445$$D View this record in MEDLINE/PubMed |
| BookMark | eNqFkV9rFDEUxYNU7Lb6FUoefZn1Jjt_MiCCLnUrbC2Igm8hk9zppswkazJTdsEPb4bd1upLnwK593cO95wzcuK8Q0IuGMwZcPZO6TjXG-wDxsHv5qIByBl7QWas4JAVwOCEzEDUi4xz8fOUnMV4B8ASW70ipwsohcjzYkZ-X-60jdY76lt6s7NGDfYeuz1docOgBjR0NSpnHdI1TnuRNnu69P0WB-tu6ScVkSpn6NdRd-gHa5A-Sn7DrbKBXqPeJInYR2odvRp75egSuy6-Ji9b1UV8c3zPyY_Pl9-XV9n6ZvVl-XGdqbwqhkznralaqBpeFMwYXmmhm_SnwECONRRtU4tGMI6tEa1osC1ULlRVg1aaKVickw8H3e3Y9Gg0uiGoTm6D7VXYS6-s_Hfi7Ebe-ntZ5mUBNU8Cb48Cwf8aU-Syt1GnE5RDP0bJWVXni7qsJ6-Lp16PJg-Rp4X3hwUdfIwBW6ntkFL3k7XtJAM5NSxTw_Jvw_LYcMLL__AHh2dBfgCn-Z0fg0uRPwf9Ac3FxkA |
| CitedBy_id | crossref_primary_10_1093_nar_gkaa777 crossref_primary_10_1016_j_dnarep_2020_102985 crossref_primary_10_3390_antiox11112110 crossref_primary_10_3390_cells8060513 crossref_primary_10_1073_pnas_1919904117 crossref_primary_10_1016_j_freeradbiomed_2019_05_037 crossref_primary_10_1039_D0CC04138F crossref_primary_10_1093_carcin_bgab087 crossref_primary_10_3390_ijms20236092 crossref_primary_10_1021_acs_chemrestox_0c00463 crossref_primary_10_1590_1678_4685_gmb_2019_0104 crossref_primary_10_1074_jbc_RA119_009834 crossref_primary_10_3390_ijms22126220 crossref_primary_10_1021_acs_biochem_0c00080 crossref_primary_10_3390_ijms22052698 crossref_primary_10_1016_j_dnarep_2021_103051 crossref_primary_10_1134_S0026893321020126 |
| Cites_doi | 10.1093/nar/29.9.1967 10.1074/jbc.M115.693218 10.1021/tx034142t 10.1016/j.dnarep.2004.07.006 10.1021/ol9913643 10.1016/j.mrfmmm.2003.09.001 10.1093/carcin/16.2.357 10.1021/bi0264925 10.1016/j.dnarep.2014.03.030 10.1093/nar/gkt1179 10.1038/nature05978 10.1038/sj.emboj.7601730 10.1021/bi800160s 10.1021/bi301566v 10.1083/jcb.200909175 10.1038/s41598-017-12963-7 10.1038/srep04894 10.1128/MCB.17.12.7069 10.1021/tx010088+ 10.1126/science.286.5446.1897 10.1016/j.dnarep.2009.11.005 10.1093/carcin/11.9.1667 10.1021/ja4059469 10.1038/35002510 10.1021/ja306077b 10.1038/nrm3822 10.1016/j.canlet.2011.12.038 10.1093/nar/24.4.596 10.1016/j.jmb.2008.12.082 10.1021/bi0017982 10.1073/pnas.89.8.3664 10.1021/acs.chemrestox.6b00265 10.1021/tx0501379 10.1021/acs.chemrestox.8b00244 10.1093/emboj/cdf350 10.1021/ja212186w 10.1021/bi901852q 10.1073/pnas.1207829109 10.1016/S1568-7864(02)00036-8 10.1021/bi981594+ 10.1021/ja962255b 10.1021/ol006993n 10.1074/jbc.M113.482257 10.1021/bi0347252 10.1093/nar/gkm1092 10.1038/nprot.2007.319 |
| ContentType | Journal Article |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
| DOI | 10.1021/acs.chemrestox.8b00411 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Public Health Pharmacy, Therapeutics, & Pharmacology |
| EISSN | 1520-5010 |
| EndPage | 761 |
| ExternalDocumentID | PMC6465092 30688445 10_1021_acs_chemrestox_8b00411 a322300920 |
| Genre | Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: NIEHS NIH HHS grantid: R01 ES027059 |
| GroupedDBID | - 29B 55A 5GY 5RE 7~N AABXI ABFLS ABMVS ABPTK ABUCX ACGFS ACJ ACS AEESW AENEX AFEFF ALMA_UNASSIGNED_HOLDINGS AQSVZ CS3 EBS ED ED~ EJD F5P GNL IH9 IHE JG JG~ LG6 P2P ROL TN5 UI2 UPT VF5 VG9 W1F X YZZ --- -~X 4.4 5VS AAYXX ABBLG ABJNI ABLBI ABQRX ADHLV AGXLV AHGAQ BAANH CITATION CUPRZ GGK CGR CUY CVF ECM EIF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-a475t-c4fd7f07b2551dd27c8cb4fda0d04e905fb98b812efd8f8bef5a48a790cac1a03 |
| IEDL.DBID | ACS |
| ISSN | 0893-228X 1520-5010 |
| IngestDate | Thu Aug 21 13:49:14 EDT 2025 Fri Jul 11 08:19:46 EDT 2025 Mon Jul 21 06:04:30 EDT 2025 Tue Jul 01 03:45:26 EDT 2025 Thu Apr 24 23:01:51 EDT 2025 Thu Aug 27 13:43:29 EDT 2020 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Language | English |
| License | https://doi.org/10.15223/policy-029 https://doi.org/10.15223/policy-037 https://doi.org/10.15223/policy-045 |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-a475t-c4fd7f07b2551dd27c8cb4fda0d04e905fb98b812efd8f8bef5a48a790cac1a03 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| ORCID | 0000-0001-8225-6509 |
| PMID | 30688445 |
| PQID | 2179439690 |
| PQPubID | 23479 |
| PageCount | 9 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_6465092 proquest_miscellaneous_2179439690 pubmed_primary_30688445 crossref_citationtrail_10_1021_acs_chemrestox_8b00411 crossref_primary_10_1021_acs_chemrestox_8b00411 acs_journals_10_1021_acs_chemrestox_8b00411 |
| ProviderPackageCode | JG~ 55A AABXI GNL VF5 7~N ACJ VG9 W1F ACS AEESW AFEFF ABMVS ABUCX IH9 AQSVZ ED~ UI2 CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2019-04-15 |
| PublicationDateYYYYMMDD | 2019-04-15 |
| PublicationDate_xml | – month: 04 year: 2019 text: 2019-04-15 day: 15 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Chemical research in toxicology |
| PublicationTitleAlternate | Chem. Res. Toxicol |
| PublicationYear | 2019 |
| Publisher | American Chemical Society |
| Publisher_xml | – name: American Chemical Society |
| References | ref9/cit9 ref45/cit45 ref6/cit6 ref36/cit36 ref3/cit3 ref27/cit27 ref18/cit18 ref11/cit11 ref25/cit25 ref16/cit16 ref29/cit29 ref32/cit32 ref23/cit23 ref39/cit39 ref14/cit14 ref8/cit8 ref5/cit5 ref31/cit31 ref2/cit2 ref43/cit43 ref34/cit34 ref37/cit37 ref28/cit28 ref20/cit20 ref17/cit17 ref10/cit10 ref26/cit26 Conney A. H. (ref40/cit40) 1982; 42 ref35/cit35 ref19/cit19 ref21/cit21 ref12/cit12 ref15/cit15 ref42/cit42 ref46/cit46 ref41/cit41 ref22/cit22 ref13/cit13 ref33/cit33 ref4/cit4 ref30/cit30 ref47/cit47 ref1/cit1 ref24/cit24 ref38/cit38 ref44/cit44 ref7/cit7 |
| References_xml | – ident: ref18/cit18 doi: 10.1093/nar/29.9.1967 – ident: ref22/cit22 doi: 10.1074/jbc.M115.693218 – ident: ref28/cit28 doi: 10.1021/tx034142t – ident: ref19/cit19 doi: 10.1016/j.dnarep.2004.07.006 – ident: ref9/cit9 doi: 10.1021/ol9913643 – ident: ref14/cit14 doi: 10.1016/j.mrfmmm.2003.09.001 – ident: ref34/cit34 doi: 10.1093/carcin/16.2.357 – ident: ref31/cit31 doi: 10.1021/bi0264925 – ident: ref2/cit2 doi: 10.1016/j.dnarep.2014.03.030 – ident: ref37/cit37 doi: 10.1093/nar/gkt1179 – ident: ref6/cit6 doi: 10.1038/nature05978 – ident: ref43/cit43 doi: 10.1038/sj.emboj.7601730 – ident: ref20/cit20 doi: 10.1021/bi800160s – ident: ref32/cit32 doi: 10.1021/bi301566v – ident: ref23/cit23 doi: 10.1083/jcb.200909175 – ident: ref25/cit25 doi: 10.1038/s41598-017-12963-7 – ident: ref24/cit24 doi: 10.1038/srep04894 – ident: ref42/cit42 doi: 10.1128/MCB.17.12.7069 – ident: ref11/cit11 doi: 10.1021/tx010088+ – ident: ref1/cit1 doi: 10.1126/science.286.5446.1897 – ident: ref46/cit46 doi: 10.1016/j.dnarep.2009.11.005 – ident: ref41/cit41 doi: 10.1093/carcin/11.9.1667 – ident: ref45/cit45 doi: 10.1021/ja4059469 – ident: ref5/cit5 doi: 10.1038/35002510 – ident: ref33/cit33 doi: 10.1021/ja306077b – ident: ref3/cit3 doi: 10.1038/nrm3822 – ident: ref7/cit7 doi: 10.1016/j.canlet.2011.12.038 – ident: ref35/cit35 doi: 10.1093/nar/24.4.596 – ident: ref44/cit44 doi: 10.1016/j.jmb.2008.12.082 – ident: ref17/cit17 doi: 10.1021/bi0017982 – ident: ref39/cit39 doi: 10.1073/pnas.89.8.3664 – ident: ref4/cit4 doi: 10.1021/acs.chemrestox.6b00265 – ident: ref12/cit12 doi: 10.1021/tx0501379 – ident: ref15/cit15 doi: 10.1021/acs.chemrestox.8b00244 – ident: ref27/cit27 doi: 10.1093/emboj/cdf350 – ident: ref30/cit30 doi: 10.1021/ja212186w – ident: ref21/cit21 doi: 10.1021/bi901852q – ident: ref13/cit13 doi: 10.1073/pnas.1207829109 – ident: ref26/cit26 doi: 10.1016/S1568-7864(02)00036-8 – volume: 42 start-page: 4875 year: 1982 ident: ref40/cit40 publication-title: Cancer Res. – ident: ref47/cit47 doi: 10.1021/bi981594+ – ident: ref8/cit8 doi: 10.1021/ja962255b – ident: ref10/cit10 doi: 10.1021/ol006993n – ident: ref38/cit38 doi: 10.1074/jbc.M113.482257 – ident: ref16/cit16 doi: 10.1021/bi0347252 – ident: ref29/cit29 doi: 10.1093/nar/gkm1092 – ident: ref36/cit36 doi: 10.1038/nprot.2007.319 |
| SSID | ssj0011027 |
| Score | 2.3703942 |
| Snippet | The interchange between different repair mechanisms in human cells has long been a subject of interest. Here, we provide a direct demonstration that the... |
| SourceID | pubmedcentral proquest pubmed crossref acs |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 753 |
| SubjectTerms | Cells, Cultured DNA Repair Fibroblasts - metabolism Guanine - chemistry Guanine - metabolism HeLa Cells Humans Kinetics Molecular Structure Oxidation-Reduction |
| Title | Excision of Oxidatively Generated Guanine Lesions by Competing Base and Nucleotide Excision Repair Mechanisms in Human Cells |
| URI | http://dx.doi.org/10.1021/acs.chemrestox.8b00411 https://www.ncbi.nlm.nih.gov/pubmed/30688445 https://www.proquest.com/docview/2179439690 https://pubmed.ncbi.nlm.nih.gov/PMC6465092 |
| Volume | 32 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1La9wwEBYhvRRKH-kj2xdTKLk03siybFnHdkkIpU1TmsDejJ7EdGOX2Au7pT--kuX1dhtC2qusEXg04_nk0XyD0Ns4YxlOmIwktjTyibOI55RHlmieJsY4kNKxfZ5kx-f04zSdbiF8QwafxAdCOeVfmEvfqqJejHNvZ76Y9w7JnCd7MDT5NuQNnETg9uRJREg-XdUE37iOD0qq2QxK15Dm3xcm_4hARw_Q11UdT7h48n08b-VY_bxO6_jPL_cQ3e_hKLwP9vMIbZlqB-2dBj7r5T6crcuzmn3Yg9M10_VyB90LP_0g1DI9Rr8OF6FjD9QWvixK3bGKz5YQyK0duAVnkpUDtvDJ-HkNyCVMOujuQih8cCEVRKXhxLMs122pDQxLuqOCKK_gs_G1ymVz2UBZQZeDgImZzZon6Pzo8GxyHPXtHSJBWdpGilrNLGbSnWpirQlTuZJuTGCNqeE4tZLn0gEQY3Vuc2lsKmguGMdKqFjg5CnarurK7CJgWMZKuQ3niUNY0pedu--mTSizxFJNRuid03TRu2dTdJl3Ehd-cK3-olf_CKUrayhUz5TuG3bMbpU7GOR-BK6QWyXerIytcG7tczWiMvW8KUjH3MczjkfoWTC-Yc3ENwqiNB0htmGWwwRPGb75pCovOurwjHrGRPL8v_TxAt11MLHLocXpS7TdXs3NKwfFWvm6877fDOc13g |
| linkProvider | American Chemical Society |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3db9MwELfQeAAJDRhf5fOQ0F5YOidxmvhxVJsKdGUSndS3KHZsEdEl05xKLeKP5-ykKR1CE7w6Piu-nHM_-3y_I-SdP4gHNIyFJ6hmng2ceTxh3NNBzqNQKQQpju1zMhids0-zaNYeXdhcGHwJgyMZF8TfsAv4h7YNp3FhK1ZUy35izc3m9N5GRBJY0z4afu3CByjRUHzy0AuCZLZODf7rONY3SbPtm_4AnNfvTf7miE7uk1k3BXf_5Ht_UYu-_HGN3fE_5viA7LbgFI4aa3pIbqlyj-yfNezWqwOYbpK1zAHsw9mG93q1R-41R4DQZDY9Ij-Pl039Hqg0fFkWueMYn6-gobpGqAtooCXCXBgr28-AWMHQAXl0qPABHSxkZQ4Ty7lc1UWuoBsSNw5ZcQWnymYuF-bCQFGCi0jAUM3n5jE5PzmeDkdeW-zBy1gc1Z5kOo81jQXucfw8D2KZSIFtGc0pU5xGWvBEIBxROk90IpSOMpZkMacyk35Gwydkp6xK9YxATIUvJX53HiLeEjYJHf-iOmSxDjTLgx55j5pO28VqUheHD_zUNm7Un7bq75FobRSpbHnTbfmO-Y1yh53cZcMccqPE27XNpbjIbeQmK1W1MGngePz4gNMeedrYYDdmaMsGMRb1SLxlnV0HSyC-_aQsvjki8QGz_InB83_SxxtyZzQ9Hafjj5PPL8hdBJAuuuZHL8lOfbVQrxCk1eK1W5C_AHjmPj8 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3ra9RAEF9KBRHER32dzxGkX2yum2Tzwk_17FG1nge2cB-EkH1h8JqU7h3ciX-8s5tczqtI0a-bnSU7mcn8ktn5DSGv_DiJaZhwj1PNPJs487KUZZ4OZBaFSiFIcWyfo_jolH2YRJMt8mZVC4M3YXAl45L41qvPpW4ZBvx9O45bObNdK-pFP7UmZ-t6r9ncnTXvg8GXLoWAEg3NZxZ6QZBOVuXBf13HxidhNuPTH6Dz8tnJ34LR8Db52m3DnUH53p_PeF_8uMTw-J_7vENutSAVDhqruku2VLVDdscNy_VyD07WRVtmD3ZhvOa_Xu6Qm82vQGgqnO6Rn4eLpo8P1Bo-L0rpuManS2gorxHyAhpqhXAXjpWdZ4AvYeAAPQZWeIuBFopKwshyL9ezUirolsQPiKK8gE_KVjCX5sxAWYHLTMBATafmPjkdHp4Mjry26YNXsCSaeYJpmWiacPzW8aUMEpEKjmMFlZSpjEaaZylHWKK0THXKlY4KlhZJRkUh_IKGD8h2VVfqEYGEcl8IfPZZiLiL22J0fJvqkCU60EwGPfIaNZ23Tmtyl48P_NwOrtWft-rvkWhlGLlo-dNtG4_plXL7ndx5wyBypcTLld3l6Ow2g1NUqp6bPHB8flmc0R552Nhht2Zo2wcxFvVIsmGh3QRLJL55pSq_OULxmFkexeDxP-njBbk-fjfMj9-PPj4hNxBHuiSbHz0l27OLuXqGWG3Gnzuf_AVb7EDC |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Excision+of+Oxidatively+Generated+Guanine+Lesions+by+Competing+Base+and+Nucleotide+Excision+Repair+Mechanisms+in+Human+Cells&rft.jtitle=Chemical+research+in+toxicology&rft.au=Shafirovich%2C+Vladimir&rft.au=Kropachev%2C+Konstantin&rft.au=Kolbanovskiy%2C+Marina&rft.au=Geacintov%2C+Nicholas+E&rft.date=2019-04-15&rft.eissn=1520-5010&rft.volume=32&rft.issue=4&rft.spage=753&rft_id=info:doi/10.1021%2Facs.chemrestox.8b00411&rft_id=info%3Apmid%2F30688445&rft.externalDocID=30688445 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0893-228X&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0893-228X&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0893-228X&client=summon |