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Oxidative DNA Damage Response in Helicobacter pylori-Infected Mongolian Gerbils

Minkyung Bae1, Joo Weon Lim1, Hyeyoung Kim1

  • 1Department of Food and Nutrition, Brian Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul, Korea.

Journal of Cancer Prevention
|October 23, 2014
PubMed

Insights

Helicobacter pylori infection causes DNA damage in gerbil stomachs, activating repair and cell death pathways. The antioxidant N-acetylcysteine (NAC) mitigated this damage, suggesting oxidative stress involvement in H. pylori-induced gastric issues.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Cancer Research

Background:

  • Helicobacter pylori (H. pylori) infection is a known risk factor for gastric cancer.
  • H. pylori-induced DNA damage is implicated in gastric carcinogenesis.
  • DNA damage response pathways, including repair, cell cycle regulation, and apoptosis, are crucial in maintaining genomic stability.

Purpose of the Study:

  • To investigate the impact of H. pylori infection on DNA damage response pathways in Mongolian gerbils.
  • To determine the role of oxidative stress in H. pylori-induced DNA damage.
  • To evaluate the protective effect of N-acetylcysteine (NAC) against H. pylori-induced DNA damage.

Main Methods:

  • Mongolian gerbils were infected with H. pylori and treated with or without N-acetylcysteine (NAC) for 6 weeks.
  • Expression levels of key DNA repair proteins (ATM, ATR, Ku70/80), cell cycle regulators (Chk1, Chk2), and apoptosis markers (p53/p-p53) were analyzed in gastric mucosa.
  • Assessment of H. pylori-induced DNA damage response and the effect of NAC.

Main Results:

  • H. pylori infection significantly increased the expression of DNA repair proteins (ATM, ATR, Ku70/80), cell cycle regulators (Chk1, Chk2), and apoptosis markers (p53/p-p53) in gerbil gastric mucosa.
  • Treatment with NAC suppressed the H. pylori-induced elevation of these DNA damage response markers.
  • These findings indicate that oxidative stress plays a mediating role in H. pylori-induced DNA damage.

Conclusions:

  • Oxidative stress is a key mechanism underlying H. pylori-induced DNA damage response in the gastric mucosa.
  • H. pylori infection triggers both non-homologous end joining (NHEJ) and homologous recombination (HR) DNA repair pathways, alongside cell cycle arrest and apoptosis.
  • NAC demonstrates a potential therapeutic role by mitigating H. pylori-induced DNA damage, likely through its antioxidant properties.
Keywords:
DNA damage responseHelicobacter pyloriMongolian gerbilOxidative stress

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