Helicobacter pylori (H. pylori)
infection plays an important role in gastric
carcinogenesis. This bacterium may induce
cancer transformation and change the susceptibility of gastric mucosa cells to various exogenous dietary irritants. The aim of the study was to evaluate the influence of H. pylori
infection on the reaction of the stomach cells to a genotoxic effect of heterocyclic
amines (HCAs). These well-known
mutagens are formed during cooking of
protein-rich foods, primarily meat. Taking into account that persons consuming a mixed-western diet are exposed to these compound nearly an entire lifetime and more than half of human population is infected with H. pylori, it is important to assess the combined effect of H. pylori
infection and HCAs in the context of DNA damage in gastric mucosa cells, which is a prerequisite to
cancer transformation. We employed 2-amino-3-methylimidazo[4,5-f]
quinoline (IQ), 2-amino-3,8-dimethyl-imidazo[4,5-f]
quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-
b]pyridine (
PhIP) because these substances are present in a great amount in cooked and fried meat. Using alkaline comet assay, we showed that the extent of the DNA damage induced by HCAs was significantly higher in H. pylori infected gastric mucosa cells than in non-infected counterparts. We did not observed any difference in the efficiency of repair of DNA lesions induced by HCAs in both type of cells.
Vitamin C reduced the genotoxic effects of HCAs in H. pylori infected and non-infected gastric mucosa cells.
Melatonin more effectively decreased DNA damage caused by HCAs in H. pylori infected gastric mucosa cells as compared with control. Our results suggest that H. pylori
infection may influence the susceptibility of gastric mucosa cells to HCAs and dietary antioxidative substances, including
vitamin C and
melatonin may inhibit the genotoxic effects of HCAs on gastric mucosa cells and may reduce the risk of
carcinogenesis caused by food borne
mutagens and H. pylori
infection.