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 c oncentrations 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 m ucosal malondialdehyde was determined by thiobarbituric acid extraction, an d gastric juice and antral mucosal ascorbic acid and total vitamin C were d etermined by high-performance liquid chromatography. Sixty-four H. pylori-p ositive patients received eradication therapy, and endoscopy was repeated a t 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 i nfection (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 < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 <mu>mol/ml; P < 0.001), and antral mucosal ascorbic acid was unchange d (48.0 versus 42.7 <mu>mol/g) in H. pylori gastritis compared with normal mucosa, Multiple regression analysis revealed that M-1-dG increased signifi cantly 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 di rectly by H. pylori.