Open AccessIncreased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor κ B expression and enhanced antiapoptosis-related proteins inHelicobacter pylori-infected non-cardiac gastric adenocarcinoma
Author(s) -
Cheng-Chen Chang,
Weina Chen,
Hui-Hsuan Lin,
Chien-Hung Wu,
ChauJong Wang
Publication year - 2004
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v10.i15.2232
Subject(s) - helicobacter pylori , nitric oxide synthase , dna damage , apoptosis , biology , cancer , oxidative stress , cancer research , microbiology and biotechnology , chemistry , nitric oxide , biochemistry , dna , endocrinology , genetics
Several epidemiological studies have demonstrated a close association between Helicobacter pylori (H pylori) infection and non-cardiac carcinoma of the stomach. H pylori infection induces active inflammation with neutrophilic infiltrations as well as production of oxygen free radicals that can cause DNA damage. The DNA damage induced by oxygen free radicals could have very harmful consequences, leading to gene modifications that are potentially mutagenic and/or carcinogenic. The aims of the present study were to assess the effect of H pylori infection on the expression of inducible nitric oxidative synthase (iNOS) and the production of 8-hydroxy-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury in human gastric mucosa with and without tumor lesions, and to assess the possible factors affecting cell death signaling due to oxidative DNA damage.