Anikeenok M O, Il'inskaia O N
Tsitologiia. 2008;50(11):1005-8.
Chronic infection with Helicobacter pylori is a factor inducing development of cancer diseases. The mechanism of its action on the "host" DNA is still not clear. In present study we investigate genotoxical potential of two strains of H. pylori: wild type H. pylori P12 and PAI-deficient mutant H. pylori deltaPAI. DNA damage was detected by DNA comet assay in gastric adenocarcinoma (AGS) and epithelial adenocarcinoma (HeLa) cells under neutral conditions using Tail Moment as a quantitative parameter. It was shown, that infection of AGS and HeLa cells with both strains H. pylori at different multiplicity of infection (20-500) for 6 h and infection of AGS for 12 h did not induce DNA damage. Our results revealed a significant dose-dependent increasing of Tail Moment in the AGS cells after infection with mutant H. pylori deltaPAI for 24 h, while genotoxity of wild type H. pylori P12 under the same conditions was not observed.
幽门螺杆菌的慢性感染是诱发癌症疾病的一个因素。其作用于“宿主”DNA的机制仍不清楚。在本研究中，我们调查了两株幽门螺杆菌的遗传毒性潜力：野生型幽门螺杆菌P12和缺乏毒力相关基因岛（PAI）的突变型幽门螺杆菌deltaPAI。在中性条件下，使用尾矩作为定量参数，通过DNA彗星试验在胃腺癌（AGS）细胞和上皮腺癌（HeLa）细胞中检测DNA损伤。结果显示，用这两株幽门螺杆菌以不同感染复数（20 - 500）感染AGS和HeLa细胞6小时以及感染AGS细胞12小时均未诱导DNA损伤。我们的结果显示，在用突变型幽门螺杆菌deltaPAI感染AGS细胞24小时后，尾矩有显著的剂量依赖性增加，而在相同条件下未观察到野生型幽门螺杆菌P12的遗传毒性。
