The Asociation of 4977-Bp Deletion of Mitochondrial Dna with Polycystic Ovary Syndrome in Iraqi Patients

Abstract

Polycystic ovarian syndrome (PCOS) is increasingly recognized as a significant health concern among women of reproductive age, exerting its influence on the reproductive system and overall female physiology. Mitochondria plays a pivotal role in generating adenosine triphosphate within human cells while also being a primary source of cellular oxidative stress. Mutation in mtDNA could influence the oxidative stress, thus the defect of PCOS. This study aims to investigate the presence of 4977-bp deletion of mitochondrial DNA in the Iraqi population and its role in PCOS.

A case-control study of 80 women with an age range (of 20- 35) years included in this study; these study populations are subdivided into two groups. Group 1: includes 40 women with PCOS. Group 2:  includes 40 age with BMI-matched women with regular menstrual cycles, no signs of hyperandrogenism, and no history of PCOS.

PCOS women demonstrated significantly higher median serum levels of FSH, LH, and Testosterone than healthy women. The results of gel electrophoresis in this study show that there were no deletions in the 4977bp of the DNA of the mitochondrial neither healthy nor PCOS women.