Mitochondrial DNA deletion Δ4977 in peptic ulcer disease
- 作者: Salehi Z.1, Haghighi A.2, Haghighi S.3, Aminian K.4, Asl S.F.4, Mashayekhi F.1
-
隶属关系:
- Department of Biology
- University of Guilan
- Department of Biology/Genetic, Tabrize Branch
- Guilan University of Medical Sciences
- 期: 卷 51, 编号 1 (2017)
- 页面: 30-33
- 栏目: Genomics. Transcriptomics
- URL: https://journal-vniispk.ru/0026-8933/article/view/162949
- DOI: https://doi.org/10.1134/S0026893317010162
- ID: 162949
如何引用文章
详细
Reactive oxygen species (ROS) play a critical role in peptic ulcer disease (PUD). Due to the high rate of ROS production and limited capacity for DNA repair within mitochondria, mtDNA is susceptible to oxidative damage and mutations. mtDNA deletion Δ4977 is one of the most common deletion events identified in mitochondria. We examined the association of 4977-bp mtDNA deletion with PUD. Genotypes were determined in bioptic samples of 150 PUD patients and 190 controls. The 4977-bp mtDNA deletion was found more frequently among patients with PUD (52%) than among controls (22.63%). The strong association between the mtDNA 4977-bp deletion and PUD was confirmed (OR = 3.7; 95% CI, 2.32–5.91; P = 0.0001). The 4977-bp deletion in mitochondrial DNA may be a risk factor for PUD, or may reflect an increase in oxidative stress that commonly accompanies underlying PUD disease. Larger population-based studies are needed to uncover the possible causal relationship between this deletion and peptic ulcer disease.
作者简介
Z. Salehi
Department of Biology
编辑信件的主要联系方式.
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Rasht
A. Haghighi
University of Guilan
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Rasht
S. Haghighi
Department of Biology/Genetic, Tabrize Branch
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Tabrize
K. Aminian
Guilan University of Medical Sciences
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Rasht
S. Asl
Guilan University of Medical Sciences
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Rasht
F. Mashayekhi
Department of Biology
Email: geneticzs@yahoo.co.uk
伊朗伊斯兰共和国, Rasht
补充文件
