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Centre for Digestive Diseases, The General Infirmary [S. M. E., K. L. M. W., P. N., C. J. S., A. T. R. A.] and Academic Unit of Epidemiology and Health Services Research, The Medical School, University of Leeds [D. G., D. F.], Leeds LS9 7TF, United Kingdom; MRC Toxicology Unit, University of Leicester, LE1 9HN Leicester, United Kingdom [R. S., C. L., D. S.]; and Centre in Molecular Toxicology, Vanderbilt University, Nashville, Tennessee 37232 [L. J. M.]
Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M1-dG). We aimed to determine gastric mucosal levels of M1-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M1-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M1-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/108 bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 µmol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 µmol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M1-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M1-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/108 bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/108 bases; P = 0.8; n = 13) after successful eradication of H. pylori. M1-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.
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