Open Access

Helicobacter pylori infection can modulate the susceptibility of gastric mucosa cells to MNNG

  • Michał Arabski1,
  • Paweł Kazmierczak2,
  • Maria Wiśniewska-Jarosińska3,
  • Zbigniew Morawiec4, 6,
  • Alina Morawiec-Bajda5,
  • Grażyna Klupińska3,
  • Józef Drzewoski5,
  • Jan Chojnacki3 and
  • Janusz Błasiak1Email author
Cellular & Molecular Biology LettersAn International Journal200611:45

https://doi.org/10.2478/s11658-006-0045-z

Received: 26 April 2006

Accepted: 22 June 2006

Published: 6 October 2006

Abstract

The pathogenesis of stomach cells can be associated with their susceptibility to exogenous dietary irritants, like nitrosamines such as dimethylnitrosamines (DMNA), and to the effects of non-dietary factors, including Helicobacter pylori infection. We used N-methyl-N’-nitro N-nitrosoguanidyne (MNNG) as a surrogate agent that induces a spectrum of DNA damage similar to DMNA. Using the alkaline comet assay, we showed that antioxidants — vitamins C and E, quercetin, and melatonin — reduced the genotoxic effect of MNNG in H. pylori-infected and non-infected human gastric mucosa cells (GMCs). To compare the sensitivity of the stomach and the blood, the experiment was also carried out in peripheral blood. We observed a higher level of DNA damage induced by MNNG in H. pylori-infected than in noninfected GMCs. We did not note any difference in the efficacy of the repair of the damage in either type of GMC. H. pylori infection may play an important role in the pathogenesis of GMCs, as it can modulate their susceptibility to dietary mutagens/carcinogens, thus contributing to gastric cancer.

Key words

Helicobacter pylori DNA damageDNA repairMNNGMelatoninVitamin CVitamin EQuercetin

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