Publication:
APE1 and XRCC3 polymorphisms and myocardial infraction

dc.contributor.authorsTekel, Atike; Isbir, Selim; Ergen, Arzu; Goermues, Uzay; Bozkurt, Niluefer; Timirci, Oezlem; Arsan, Sinan; Isbir, Turgay
dc.date.accessioned2022-03-12T17:34:20Z
dc.date.accessioned2026-01-11T13:54:26Z
dc.date.available2022-03-12T17:34:20Z
dc.date.issued2008
dc.description.abstractBackground: In most cells, DNA is regularly damaged by mutagens. Different DNA repair mechanisms operate on specific types of damaged DNA. When DNA damage resulting from free radicals is not repaired, it might lead to deteriorated gene expression, the development of a number of diseases such as cancer, diabetes, vascular diseases, and aging. In the present study, APE1 and XRCC3 gene polymorphisms were investigated in patients with myocardial infarction. Materials and Methods: Forty-five first time elective coronary artery bypass grafting (CABG) patients with cardiopulmonary bypass (CPB) and 40 healthy individuals were studied. Gene polymorphisms were determined by a polymerase chain reaction-restriction fragment length polymorphism method. Results: For the APE1 gene, the AG genotype was significantly higher in the patient group than in the control group. The patient group had significantly more G carriers but there was no statistically significant difference between patient and control groups the A allele. The XRCC3 TT genotype was found to be significantly more frequent in the patient group than it was in the control group. Conclusion: The results of our study suggested that the XRCC3 gene TT genotype and the APE1 gene AG genotype might increase the risk of myocardial infarcts.
dc.identifier.doidoiWOS:000257861100012
dc.identifier.issn0258-851X
dc.identifier.pubmed18712175
dc.identifier.urihttps://hdl.handle.net/11424/229007
dc.identifier.wosWOS:000257861100012
dc.language.isoeng
dc.publisherINT INST ANTICANCER RESEARCH
dc.relation.ispartofIN VIVO
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectDNA damage
dc.subjectcoronary artery disease
dc.subjectoxidative stress
dc.subjectDNA repair
dc.subjectgene
dc.subjectIONIZING-RADIATION SENSITIVITY
dc.subjectAPURINIC/APYRIMIDINIC ENDONUCLEASE
dc.subjectBLADDER-CANCER
dc.subjectDNA
dc.subjectREPAIR
dc.subjectDAMAGE
dc.subjectCELLS
dc.subjectRISK
dc.subjectBREAKS
dc.titleAPE1 and XRCC3 polymorphisms and myocardial infraction
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage479
oaire.citation.issue4
oaire.citation.startPage477
oaire.citation.titleIN VIVO
oaire.citation.volume22

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