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Investigation of APE1 and OGG1 expression in chronic hemodialysis patients

Background The role of DNA repair mechanisms is of significant importance in diseases characterized by elevated oxidative DNA damage, such as chronic kidney disease. It is imperative to thoroughly understand the functions of molecules associated with DNA repair mechanisms, not only for assessing sus...

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Published in:Molecular biology reports 2024-12, Vol.51 (1), p.144-144, Article 144
Main Authors: Rostami, Manouchehr, Yalin, Serkan Feyyaz, Altiparmak, Mehmet Riza, Guven, Mehmet
Format: Article
Language:English
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Summary:Background The role of DNA repair mechanisms is of significant importance in diseases characterized by elevated oxidative DNA damage, such as chronic kidney disease. It is imperative to thoroughly understand the functions of molecules associated with DNA repair mechanisms, not only for assessing susceptibility to diseases but also for monitoring disease progression. In this research, we investigated the APE1 and OGG1 gene expression levels, both of which are involved in the base excision repair (BER) mechanism in chronic hemodialysis patients with malignancy (HPM; n = 8) and without malignancy (HP; n = 36) in pre- and post-dialysis period and 37 healty persons. We also assessed how these values correlate with the clinical profiles of the patients. Methods and results We conducted gene expression analysis using real-time polymerase chain reaction (qRT-PCR). No significant differences in APE1 gene expression levels were observed in pre-dialysis when comparing the HP and HPM groups to the control group. The expression levels of the OGG1 gene were significantly lower in both the HP and HPM groups in pre- and post-dialysis periods compared to the control group. Dialysis procedures led to a reduction in APE1 and OGG1 gene expression levels in both HP and HPM groups. Conclusions The findings of our study elucidate the impact of alterations in the base excision repair (BER) mechanism, including the hemodialysis process, in end-stage renal disease (ESRD).
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-023-09152-3