Protective action of melatonin and quercetin against DNA damage induced by N-methyl-N'-nitro-N-nitrosoguanidine in normal and Helicobacter pylori-infected gastric mucosa cells
Journal Title: Gastroenterologia Polska - Year 2006, Vol 13, Issue 4
Abstract
Introduction: Helicobacter pylori (H. pylori) infection is a predominant factor of chronic gastritis and is believed to contribute to distal gastric cancer development. The pathogenesis of the disease in stomach cells is associated with their susceptibility to exogenous dietary irritants, like N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and non-dietary factors, mainly H. pylori infection. The infection is a source of free radicals produced by neutrophils causing an increase of gastric mucosal lipid peroxidation product levels and DNA damage of the host. Aim of study: The aim of our investigation was to estimate the effect of melatonin and quercetin on genotoxic activity of MNNG in H. pylori-infected and non-infected gastric mucosa cells (GMCs). At the same time DNA damage and repairwas determined in peripheral blood lymphocytes (PBLs) in order to compare their sensitivity with GMCs. Material and methods: The study was conducted on 18 H. pylori-infected patients with a positive 13C-urea breath test and 22 non-infected con-trols. DNA damage was determined by comet assay in the presence of MNNG alone and after the addition of antioxidants: melatonin and quercetin. In GMCs and PBLs we also evaluated kinetics of DNA repair after inducing its damage by MNNG and hydrogen peroxide (H202). Results: The extent of DNA damage evoked by H. pylori (5.02±0.39) and by MNNG at 1 umol/L (5.92±0.28) or 5 umol/L (10.52±0.45) in non-infected GMCs are approximately on the similar level like induced by MNNG in H. pylori infected GMCs (7.90±0.33 for 1 umol/L and 17.54±0.59 for 5 umol/L). Melatonin reduced DNA damage induced by MNNG in PBLs by up to 83%, in non-infected GMCs by up to 70% and in H. pylori-infected GMCs by up to 86%. The DNA protective effect of quercetin was not that prominent comparing to melatonin. It reduced DNA damage by 17% in PBLs. In non-infected GMCs the maximal reduction was by 45%.The reduction was observed only with higher MNNG concentration in PBLs and H. pylori negative GMCs. In H. pylon-infected GMCs quercetin reduced DNA damage by 56%. No difference was observed in the efficacy of the repair of the MNNG-damaged DNA in infected and non-infected GMCs. Conclusions: H. pylori infection may play an important role in the pathogenesis of GMCs in the context of their susceptibility to dietary mutagens. This effect can be reduced by melatonin and quercetin.
Authors and Affiliations
Grażyna Klupińska, Michał Arabski, Maria Wiśniewska-Jarosińska, Józef Drzewoski, Janusz Błasiak, Jan Chojnacki
Keywords
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