Abstract

Objectives: At this study, it is aimed to research DNA damage and oxidative stress in infants with born timely normal spontaneous vaginal delivery (NSVD) and elective caesarean.Study Design: Healthy term babies born with NSVD (n=36) and elective caesarean section (n = 36) were included in the study. Determination of DNA damage was studied in fresh heparinized blood by the Comet Assay (mononuclear cell alkaline electrophoresis) method. Total oxidant capacity and total antioxidant capacity values were measured by using Erel method (colorimetric) on study day by autoanalysers and oxidative stress index values were calculated.Results: Mean total oxidant capacity, oxidative stress index and DNA damage values were significantly higher in babies born with NSVD compared to those born with elective cesarean section (p <0.001, p<0.001, p<0.001, respectively). Serum total antioxidant capacity values were not statistically significant (p=0.127).Conclusion: In this study, oxidative stress and DNA damage values of babies born with NSVD were found to be higher than those born by elective cesarean section. This suggests that there may be a relationship between the mode of delivery and oxidative stress, and that increased oxidative stress may also lead to DNA damage.

Highlights

  • In biological systems, a molecule that gains an electron is called anti-oxidant or free radical

  • Mean total oxidant capacity, oxidative stress index and DNA damage values were significantly higher in babies born with normal spontaneous vaginal delivery compared to those born with elective cesarean section (p

  • In this study, oxidative stress and DNA damage values of babies born with normal spontaneous vaginal delivery were found to be higher than those born by elective cesarean section

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Summary

Introduction

A molecule that gains an electron is called anti-oxidant or free radical. Reduction in anti-oxidants against oxidants and/or increase in oxidants can be defined as oxidative stress. Free radicals destroy the structure and function of the target molecules by taking an electron away [1,2]. Increase in generation of reactive oxygen metabolites, decrease in anti-oxidant enzyme levels and/or defect DNA repair mechanisms lead to an increase in oxidative stress and ulti-. Quick Response Code: Access this article online. How to cite this article: Kazanasmaz H. and Abuhandan M. The cell responds to DNA damage via various metabolic ways [6]. Serious DNA damages activate the apoptosis mechanism of the cell and eventually kill it. The cell is able to repair this damage by “DNA repair mechanism”. If the DNA damage remains unrepaired, it leads to mutations and genomic instability, malignancy, and aging

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