OBJECTIVE: Helicobacter pylori infection causes gastric diseases, but the r
esponsible mechanisms are not completely understood. They can involve DNA a
nd tissue damage induced by reactive oxygen and nitrogen species. Our aim i
s to investigate the effects of bacterial eradication on oxidative stress b
y measuring changes of relevant markers.
METHODS: Antral biopsies were obtained from 34 patients with chronic atroph
ic gastritis and peptic ulcer disease before and after bacterial eradicatio
n. The expression of inducible nitric oxide synthase (iNOS) and levels of n
itrotyrosine (NTYR) and 8-hydroxy-2 ' -deoxyguanosine were assessed immunoh
istochemically as markers of nitric oxide (NO) production and of damage to
proteins and DNA, respectively.
RESULTS: Before treatment, the percentages of patients with staining were:
56 for iNOS in inflammatory cells, 79 and 61 for NTYR and 8-hydroxy-2 ' -de
oxyguanosine in foveolar cells, respectively, and 82 for 8-hydroxy-2 ' -deo
xyguanosine in lymphoid follicles. NTYR staining was associated with the in
tensity of inflammation (p = 0.04) and gastritis activity (p = 0.07). The p
revalence of 8-hydroxy-2 ' -deoxyguanosine tended to be associated with tha
t of NTYR. After successful H. pylori eradication, the prevalence of iNOS a
nd NTYR (in mild gastritis) staining decreased (p < 0.001 and p < 0.06, res
pectively). 8-Hydroxy-2 ' -deoxyguanosine staining disappeared in 24% of ca
ses but appeared in 18% of previously negative cases despite eradication.
CONCLUSION: Targets of oxidative stress associated with H. pylori infection
are inflammatory and deep foveolar cells and lymphoid follicles. This is t
he first report of 8-hydroxy-2 ' -deoxyguanosine localization in gastric mu
cosa. Oxidative stress is reduced by bacterial eradication in the first sta
ges of mild gastritis. Moderate-severe gastritis may be a step that is reve
rsible for iNOS, but partly irreversible for NTYR and 8-hydroxy-2 ' -deoxyg
uanosine. (C) 2001 by Am. Cell. of Gastroenterology.