Gut and Liver, Vol. 5, No. 3, September 2011, pp. 315-320 ORiginal Article Relationship between the Extent of DNA Damage and Gastritis in Normal and Helicobacter pylori -Infected Patients Mohammed Ali M. Marie* and Isam Elshaikh Altahir† *Clinical Laboratory Department, King Saud University, College of Applied Medical Sciences, and Clinical Laboratory Department, King Saud University Riyadh, College of Health Sciences, Riyadh, Saudi Arabia Background/Aims: The role of Helicobacter pylori in gastric carcinogenesis is unclear, but H. pylori infection is thought to predispose carriers to gastric cancer. The aim of this study was to investigate the relationship between the extent of DNA damage in normal gastric epithelial cells and H. pylori- positive and -negative gastritis according to histological diag- nosis. We also compared the percentage of cometed cells on the surface of the gastric epithelial cells to the percentage beneath the gastric mucosal cells using serial incubations times. Methods: The comet assay is a rapid, efﬁcient and re- producible measure of DNA damage in single cell and it was used in this study. DNA damage was evaluated in 52 cases using alkaline single cell gel electrophoresis (comet assay). Comparisons were made between 19 normal individuals, 19 patients with H. pylori-positive and -negative gastritis and 14 mixed cases with different histology gradings to determine if there was a relationship between histological diagnosis and DNA damage (comet percentage). Results: The comet percentages in specimens from cases with normal histol- ogy were signiﬁcantly higher than the comet percentages in specimens from cases with H. pylori-positive gastritis. In ad- dition, there was a signiﬁcant increase in the percentage of cometed cells on the surface of gastric epithelial cells in both normal and H. pylori-infected cells compared to the subse- quent gastric cell layers of the same specimen. Conclusions: A relationship between the comet percentage and the histo- logical diagnosis was observed. (Gut Liver 2011;5:315-320) Key Words: Comet assay; Helicobacter pylori; Gastric cancer INTRODUCTION Gastric cancer is the second most common malignancy in the world, accounting for 9.9% of all cancer incidence and 12.1% of all cancer death.1 Carcinogenesis is a multistep process and steps involved on it relate to initiation-promotion sequences. Initiation cause permanent DNA damage (mutation). It is there- fore potentially leads to cancer development. Promoters can induce tumours in initiated cells, but they are non-tumourgenic by themselves.2 Gastritis and Helicobacter pylori are considered to be risk factors for gastric carcinoma.3 There is growing evi- dence supporting an association between H. pylori and gastric cancer. H. pylori infection induces chronic inflammation that can progress to gastric atrophy, intestinal metaplasia and gastric adenocarcinoma.4 The objective of this study is to investigate the relationship between the extent of DNA damage and the histological grad- ing of the gastric epithelium from which the biopsy was taken. Secondly for the comparison of percentages of gastric epithelia cells of H. pylori-positive and -negative gastritis with the nor- mal gastric cells. Finally the study compared the percentages of DNA damaged on the surface of gastric epithelial cells with the cells underneath in both normal individuals and patients with H. pylori-positive and -negative gastritis patients. MATERIALS AND METHODS The study population consisted of 52 unselected patients at- tending endoscopy clinic suffering from dyspepsia at Al Iman General Hospital, Riyadh, Saudi Arabia. At endoscopy unit, biop- sies were taken from the gastric antrum for histopathology and for H. pylori urease testing. After the comet and histopathology were performed, we selected and compared the results showing the per- centages of DNA damage of gastric cells of 19 normal individuals with 19 patients with positive and negative H. pylori gastritis and 14 cases of different histological diagnosis were tested. Correspondence to: Mohammed Ali M. Marie Clinical Laboratory Department, King Saud University College of Applied Medical Sciences, P.O. Box 10219, Riyadh 11433, Saudi Arabia Tel: +96614696022, Fax: +96614693738, E-mail: mmarie@ksu.edu.sa Received on November 9, 2010. Accepted on March 13, 2011. pISSN 1976-2283 eISSN 2005-1212 http://dx.doi.org/10.5009/gnl.2011.5.3.315 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.