Volume 22, Issue 88 (1-2014)                   JGUMS 2014, 22(88): 1-6 | Back to browse issues page

XML Persian Abstract Print


1- University of Guilan, Faculty of Sciences
2- University of Guilan, Faculty of Sciences , zibazahirisorouri@yahoo.com
Abstract:   (6990 Views)
Abstract Introduction: Spontaneous abortion is a pregnancy ending with the death of fetus prior to 20th week. About 30-50% of human conceptions end in spontaneous abortion and most of them occur at the time of implantation in association with oxidative stress, which can damage mitochondrial DNA (mtDNA). Defective respiratory chain enzymes, encoded by deleted mtDNA, may further enhance oxidative damage. Objective: Analysis of mtDNA common deletion (4977-bp) in women with spontaneous abortion. Materials and methods: Genomic DNA was extracted from the blood samples of 150 women with spontaneous abortion and 90 controls then, subjected to the Gap-PCR technique. A pair of primers designed by means of oligo7 software to flank the region of the mitochondrial genome where the common deletion occurs, was employed. Statistical analysis was performed using MedCalc software. Results: As revealed, 45 (30%) of women with spontaneous abortion had 4977-bp deletion in mtDNA, while only 6 (6.66%) of the controls were with the deletion. We found that 4977-bp deletion was significantly associated with increased risk of spontaneous abortion (OR= 6.00, 95% confidence interval (CI) = 2.44-14.74, P= 0.0001). Conclusion: Overall, a strong association between 4977-bp deletion and spontaneous abortion was observed. However, larger population-based studies are needed to further evaluate the relationship between this deletion and spontaneous abortion. Conflict of interest: non declared
Full-Text [PDF 363 kb]   (2125 Downloads)    
Review Paper: Research | Subject: Special
Received: 2014/01/5 | Accepted: 2014/01/5 | Published: 2014/01/5

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.