Analysis of cell damage in Helicobacter pylori-associated gastritis

Kenji Noguchi, Katsuaki Kato, Takuya Moriya, Takashi Suzuki, Michiya Saito, Tohru Kikuchi, Jing Yang, Akira Imatani, Hitoshi Sekine, Syuichi Ohara, Takayoshi Toyota, Tooru Shimosegawa, Hironobu Sasano

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)110-118
Number of pages9
JournalPathology international
Volume52
Issue number2
DOIs
Publication statusPublished - 2002

Keywords

  • Anti-oxidants
  • ELISA
  • Helicobacter pylori
  • Immunohistochemistry
  • Oxidative stress
  • Stomach
  • Superoxide dismutase

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Fingerprint Dive into the research topics of 'Analysis of cell damage in Helicobacter pylori-associated gastritis'. Together they form a unique fingerprint.

  • Cite this

    Noguchi, K., Kato, K., Moriya, T., Suzuki, T., Saito, M., Kikuchi, T., Yang, J., Imatani, A., Sekine, H., Ohara, S., Toyota, T., Shimosegawa, T., & Sasano, H. (2002). Analysis of cell damage in Helicobacter pylori-associated gastritis. Pathology international, 52(2), 110-118. https://doi.org/10.1046/j.1440-1827.2002.01331.x