REACTIVE OXYGEN SPECIES ACTIVITY AND LIPID-PEROXIDATION IN HELICOBACTER-PYLORI-ASSOCIATED GASTRITIS - RELATION TO GASTRIC-MUCOSAL ASCORBIC-ACID CONCENTRATIONS AND EFFECT OF HELICOBACTER-PYLORI ERADICATION
Im. Drake et al., REACTIVE OXYGEN SPECIES ACTIVITY AND LIPID-PEROXIDATION IN HELICOBACTER-PYLORI-ASSOCIATED GASTRITIS - RELATION TO GASTRIC-MUCOSAL ASCORBIC-ACID CONCENTRATIONS AND EFFECT OF HELICOBACTER-PYLORI ERADICATION, Gut, 42(6), 1998, pp. 768-771
Background-Helicobacter pylori is an independent risk factor for gastr
ic cancer, and this association may be due to the bacterium causing re
active oxygen species mediated damage to DNA in the gastric epithelium
, High dietary ascorbic acid intake may protect against gastric cancer
by scavenging reactive oxygen species. Aims-To assess reactive oxygen
species activity and damage in gastric mucosa in relation to gastric
pathology and mucosal ascorbic acid level, and to determine the effect
of H pylori eradication on these parameters. Patients-Gastric biopsy
specimens were obtained for analysis from 161 patients undergoing endo
scopy for dyspepsia. Methods-Reactive oxygen species activity and dama
ge was assessed by luminol enhanced chemiluminescence and malondialdeh
yde equivalent estimation respectively. Ascorbic acid concentrations w
ere measured using HPLC. Results-Chemiluminescence and malondialdehyde
levels in gastric mucosa were higher in patients with H pylori gastri
tis than in those with normal histology. Successful eradication of the
bacterium led to decreases in both parameters four weeks after treatm
ent was completed. Gastric mucosal ascorbic acid and total vitamin C c
oncentrations were not related to mucosal histology but correlated wea
kly with reactive oxygen species activity (chemiluminescence and malod
ialdehyde levels). Conclusions-Data suggest that reactive oxygen speci
es play a pathological role in H pylori gastritis, bur mucosal ascorbi
c acid is not depleted in this condition.