Gene‐specific oxidative DNA damage in Helicobacter pylori–infected human gastric mucosa

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Abstract
To study the status of oxidative DNA damage in Helicobacter pylori infection in more detail, we examined oxidative DNA damage to individual genes by determining the loss of PCR product of a targeted gene before and after gastric mucosal DNA was treated with 8‐hydroxyguanine glycosylase, which cleaves DNA at the 8‐hydroxyguanine residues. The results showed that, of the 5 genes tested, p53, insulin‐like growth factor II receptor and transforming growth factor‐β receptor type II showed significant oxidative DNA damage in H. pylori‐positive tissues and that the BAX and β‐ACTIN genes were relatively undamaged. These results suggest that in H. pylori infection, oxidative DNA damage does not occur homogeneously throughout the genomic DNA but, rather, in a gene‐specific manner. We conclude that the progressive accumulation of preferential oxidative DNA damage in certain genes, such as p53, likely contributes to gastric carcinogenesis.