F. Farinati et al., GASTRIC ANTIOXIDANT, NITRITES, AND MUCOSAL LIPOPEROXIDATION IN CHRONIC GASTRITIS AND HELICOBACTER-PYLORI INFECTION, Journal of clinical gastroenterology, 22(4), 1996, pp. 275-281
We have evaluated gastric juice pH, nitrites and vitamin C levels, muc
osal glutathione, and malondialdehyde, a marker of lipid peroxidation,
in patients with chronic gastritis undergoing endoscopy. Patients had
chronic gastritis with (n = 28) or without (n = 60) atrophy and/or co
ncomitant Helicobacter pylori infection. Nineteen healthy subjects, wi
thout major macroscopic or histologic changes, were included as contro
ls. Ten subjects were studied before and after H. pylori eradication.
Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pyl
ori infection (p < 0.02). Nitrite concentrations and pH were significa
ntly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover wa
s higher than normal in gastritis, with higher levels of oxidized glut
athione (p < 0.02). Gastric malondialdehyde levels were significantly
increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05).
Overall, more active gastritis coincided with lower vitamin C levels a
nd higher malondialdehyde levels. After H. pylori eradication a drop i
n mucosal MDA levels was observed (p = 0.04). In summary, chronic gast
ritis and H. pylori infection correlate with increased free-radical pr
oduction, reduced gastric vitamin C levels, and increased glutathione
turnover. The possible implications of these changes in the pathogenes
is of gastric damage and in carcinogenesis are intriguing.