Levels of malondialdehyde-deoxyguanosine in the gastric mucosa: relationship with lipid peroxidation, ascorbic acid, and Helicobacter pylori.

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 (M 1 -dG). We aimed to determine gastric mucosal levels of M 1 -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 M 1 -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 M 1 -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/10 8 bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P versus 15.0 μmol/ml; P versus 42.7 μmol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M 1 -dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M 1 -dG levels were unchanged 6 months (63.3 versus 87.0 adducts/10 8 bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/10 8 bases; P = 0.8; n = 13) after successful eradication of H. pylori. M 1 -dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori .