320 Gut and Liver, Vol. 5, No. 3, September 2011 tients compared to normal individuals. In summary, the results of this study have shown that in nor- mal individuals the high degree of DNA damage from the sur- face epithelium of gastric mucosa could be due to the fact that these cells are older and accumulate damaged DNA with age. If cells are undergoing DNA damage as a result of physiological cell death, then DNA repair mechanisms will not be activated. The process leading to cell death is slower in normal cells, giv- ing more time for DNA damage to be measured experimentally. This may explain the high degree of DNA damage from the surface epithelium of the gastric mucosa in normal individuals. In H. pylori, the low degree of DNA damage from the surface epithelium of the gastric mucosa could be due to rapid turnover of the epithelial cells as a result of inflammatory response and hence younger cells with low DNA damage are present in the gastric mucosa. Increased rates of cellular exfoliation and cell proliferation have been demonstrated in tissues infected with H. pylori.9 In H. pylori patients some gastric cells with DNA damage may not be included in the biopsy specimen, and if they have a high degree of DNA damage they are more likely to die or be phagocytosed by immune cells. Therefore, part of the gastric cells with DNA damage might not be detected in H. pylori infected tissue. This may explain the low degree of DNA damage from the surface epithelium of gastric mucosa in H. pylori patients. In conclusion, there was a relationship between comet per- centage and histological diagnosis. Comet percentages in speci- mens from case with normal histology were significantly higher than comet percentages in specimen from case with H. pylori gastritis. Finally, there was a significant increase in the percent- ages of surfaced cometed gastric epithelial cells compared to the subsequent gastric epithelial cells and the following gastric lay- ers. CONFLICTS OF INTEREST No potential conflict of interest relevant to this article was reported. ACKNOWLEDGEMENTS We would like to thank all the staff at Research Center, Col- lege of Applied Medical Sciences, King Saud University for their valuable support. REFERENCES 1. Shen H, Wang X, Hu Z, et al. Polymorphisms of DNA repair gene XRCC3 Thr241Met and risk of gastric cancer in a Chinese popula- tion. Cancer Lett 2004;206:51-58. 2. Crawford JM. The gastrointestinal tract: liver, biliary tract, and pancreas. In: Robbins SL, Cotran RS, Kumar V, eds. Robbins pathologic basis of disease. 4th ed. Philadelphia: W.B. Saunders, 1991. 3. Haenszel W, Kurihara M, Segi M, Lee RK. Stomach cancer among Japanese in Hawaii. J Natl Cancer Inst 1972;49:969-988. 4. Ladeira MS, Rodrigues MA, Salvadori DM, Queiroz DM, Freire- Maia DV. DNA damage in patients infected by Helicobacter pylori. Cancer Epidemiol Biomarkers Prev 2004;13:631-637. 5. Singh NP, McCoy MT, Tice RR, Schneider EL. A simple technique for quantitation of low levels of DNA damage in individual cells. Exp Cell Res 1988;175:184-191. 6. Olive PL, Wlodek D, Banáth JP. DNA double-strand breaks mea- sured in individual cells subjected to gel electrophoresis. Cancer Res 1991;51:4671-4676. 7. Arabski M, Klupinska G, Chojnacki J, et al. DNA damage and repair in Helicobacter pylori-infected gastric mucosa cells. Mutat Res 2005;570:129-135. 8. Cerutti PA. Oxy-radicals and cancer. Lancet 1994;344:862-863. 9. Asaka M, Kimura T, Kato M, et al. Possible role of Helicobacter pylori infection in early gastric cancer development. Cancer 1994;73:2691-2694. 10. Dixon MF. Pathophysiology of Helicobacter pylori infection. Scand J Gastroenterol Suppl 1994;201:7-10. 11. Halliwell B, Aruoma OI. DNA damage by oxygen-derived species: its mechanism and measurement in mammalian systems. FEBS Lett 1991;281:9-19. 12. Crabtree JE, Wyatt JI, Sobala GM, et al. Systemic and mucosal humoral responses to Helicobacter pylori in gastric cancer. Gut 1993;34:1339-1343.