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Clinical Chemistry 53: 1390-1392, 2007; 10.1373/clinchem.2007.088047
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(Clinical Chemistry. 2007;53:1390-1392.)
© 2007 American Association for Clinical Chemistry, Inc.

Letters to the Editor

Association between Helicobacter pylori–Related Peptic Ulcer Tissue and Somatic Mitochondrial DNA Mutations

Soong Lee1, Myung-Geun Shin2,a, Won-Hyeong Jo2, Mi-Ji Kim3, Hye-Ran Kim3, Wan-Sik Lee4, Dong-Ho Park1, Jong-Hoon Won1, Jong-Hee Shin2, Soon-Pal Suh2 and Dong-Wook Ryang2

1 Department of Internal Medicine, College of Medicine, Seonam University, Namwon, South Korea
Departments of2 Laboratory Medicine, and 4 Gastroenterology, Chonnam National University, Medical School and, Chonnam National University, Hwasun Hospital, Hwasun, South Korea
3 Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, South Korea

aAddress correspondence to this author at: Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun, Hospital, 160 Ilsimri, Hwasun-eup, Hwasun-gun, Jeollanam-do 519-809, South Korea. Fax 82-61-379-7984; e-mail mgshin@chonnam.ac.kr.

The first 20% of the full text of this article appears below.


To the Editor:

Mitochondrial DNA (mtDNA) is particularly susceptible to oxidative damage and mutations because of the high level of reactive oxygen species (ROS) generated and the inefficiency of the mtDNA repair system. Although the limited repair capacity hypothesis has been validated experimentally in some experimental systems, recent data have shown the existence of base excision repair mechanisms in mammalian mtDNA (1). ROS are commonly released in gastric mucosa inflamed as a result of Helicobacter pylori infection. It is postulated that mtDNA mutations arise in inflamed or chronically damaged gastroduodenal epithelial cells. Therefore, we investigated mtDNA alterations in 25 matched peptic ulcer tissue specimens associated with H. pylori infection, blood samples, and 5 nonulcer tissue samples. The study received institutional review board approval, and all participants gave informed consent.

We used a published protocol to sequence the mtDNA control region and cytochrome b (Cytb) gene and to determine the . . . [Full Text of this Article]






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Copyright © 2007 by the American Association for Clinical Chemistry.