Helicobacter pylori infection and antioxidants can modulate the genotoxic effects of heterocyclic amines in gastric mucosa cells

Tomasz Poplawski,Cezary Chojnacki,Anna Czubatka,Grazyna Klupinska,Janusz Blasiak,Jan Chojnacki

doi:10.1007/s11033-013-2622-3

Tomasz Poplawski, Cezary Chojnacki + Show 4 more

Open Access

https://doi.org/10.1007/s11033-013-2622-3

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Abstract

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.

Highlights

Helicobacter pylori (H. pylori) is a gram-negative, spiralshaped bacterium that colonize the stomach in more than half of the world population
Our results suggest that H. pylori infection may influence the susceptibility of gastric mucosa cells to heterocyclic amines (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
In the present work we wanted to assess, whether H. pylori infection may modulate the response of gastric mucosa cells to dietary mutagens, HCAs, and whether the infection affect the action of known free radicals scavengers, vitamin C and melatonin

Summary

Introduction

Helicobacter pylori (H. pylori) is a gram-negative, spiralshaped bacterium that colonize the stomach in more than half of the world population This bacterium has been classified as a definite carcinogen for gastric cancer by the International Center for Cancer Research on the basis of numerous epidemiological studies [1]. It was reported that CagA-negative H. pylori strains could initiate cancer transformation, but the mechanisms of carcinogenesis in this case is associated with chronic gastritis. In this inflammatory condition the immune cells try to kill bacterial cells and synthesize large amounts of free radicals and aldehydes and gastric cells are exposed to these radicals, gastric juice, N-nitroso compounds, which are thought to play a secondary, after CagA, role in the development of gastric cancer associated with H. pylori infection [2].

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