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Vol 51(2017) N 1 p. 30-33; DOI 10.1134/S0026893317010162  Z. Salehi1*, A. Haghighi2, S. Haghighi3, K. Aminian4, S.F. Asl4, F. Mashayekhi1 Mitochondrial DNA deletion Δ4977 in peptic ulcer disease 1Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran2University of Guilan, University campus 2, Rasht, Iran 3Department of Biology/Genetic, Tabrize Branch, Islamic Azad University, Tabrize, Iran 4Guilan University of Medical Sciences, Rasht, Iran *geneticzs@yahoo.co.uk Received - 2015-11-16; Accepted - 2016-01-12 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. peptic ulcer disease, mtDNA deletion, oxidative stress |
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