Increased oxidative DNA damage in Helicobacter pylori-infected human gastric mucosa

Helicobacter pylori causes type B gastritis. It shows strong association with the development of gastric carcinoma. A plausible hypothesis for the missing link between H. pylori infection and gastric carcinogenesis involves oxygen free radical-induced DNA damage. To test this hypothesis, we compared...

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Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 1996-03, Vol.56 (6), p.1279-1282
Hauptverfasser: SEUNG-CHUL BAIK, HEE-SHANG YOUN, MYUNG-HEE CHUNG, WOO-KON LEE, MYUNG-JE CHO, GYUNG-HYUCK KO, CHEOL-KEUN PARK, KASAI, H, KWANG-HO RHEE
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Sprache:eng
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Zusammenfassung:Helicobacter pylori causes type B gastritis. It shows strong association with the development of gastric carcinoma. A plausible hypothesis for the missing link between H. pylori infection and gastric carcinogenesis involves oxygen free radical-induced DNA damage. To test this hypothesis, we compared the amount of 9-hydroxydeoxyguanosine, a marker for oxygen free radical-induced DNA damage, in the DNA of human gastric mucosa with and without H. pylori infection. Gastric antral biopsies were taken from pediatric patients and volunteers to select H. pylori-positive and H. pylori-negative specimens. The 8-hydroxydeoxyguanosine content of the gastric mucosal DNA was measured after H. pylori-positive and H. pylori-negative volunteers were identified. The increased level of oxidative DNA damage suggests the mechanistic link between H. pylori infection and gastric carcinoma.
ISSN:0008-5472
1538-7445