Helicobacter pylori
infection is currently considered to be a major cause of acute and chronic
gastritis, and of gastric and
duodenal ulcers.
Superoxide dismutase (SOD) is well known for scavenging
superoxide radicals such as
reactive oxygen species (ROS), subsequently protecting cells from oxidative injury, and for maintaining tissue homeostasis. In this study, we therefore evaluated the level of SOD activity and
protein expression, as well as various factors associated with oxidative injury, in H. pylori-positive (n = 46) and -negative (n = 28) gastric mucosa obtained from endoscopy, in order to elucidate the possible
biological significance of SOD in these mucosa. Overall SOD activity was significantly higher in H. pylori-positive mucosa (15.5 +/- 7.0 U/mg
protein) than in negative mucosa (9.2 +/- 10.6 U/mg
protein), and decreased markedly following H. pylori eradication (8.2 +/- 4.2 U/mg
protein).
Enzyme-linked
immunosorbent assay (ELISA) analysis of SOD revealed that the
manganese SOD (
Mn-SOD) level in H. pylori-positive mucosa (1166.7 +/- 435.2 ng/mg
protein) was significantly higher than in control tissues (446.3 +/- 435.3 ng/mg
protein) and in mucosa obtained following eradication
therapy (431.9 +/- 189.9 ng/mg
protein). The level of
Mn-SOD protein showed a significant correlation with degree of
inflammation in the gastric mucosa. Moreover,
Mn-SOD immunolocalization patterns were well correlated with the activity and
protein levels evaluated by ELISA. Factors presumably associated with oxidative injury in human gastric mucosa, including
terminal deoxynucleotidyl transferase-mediated dUTP-
biotin nick-end labeling, Ki-67,
8-hydroxydeoxyguanosine and
single-stranded DNA, were all significantly higher in H. pylori-positive gastric mucosa than in control tissue and in tissue following eradication. These results all suggest that
Mn-SOD, but not cytoplasmic
copper-
zinc SOD, plays an important role as an
anti-oxidant against ROS generated in H. pylori-infected gastric mucosa and, subsequently, in the maintenance of cell turnover in gastric mucosa.