Ammonia aggravates stress-induced gastric mucosal oxidative injury through the cancellation of cytoprotective heat shock protein 70

Shoichi Nagahashi, Hidekazu Suzuki, Masaharu Miyazawa, Hiroshi Nagata, Masayuki Suzuki, Soichiro Miura, Hiromasa Ishii

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The relationship between Helicobacter pylori colonization and the formation of stress-induced gastric mucosal injury remains unknown. Since ammonia (NH3) is known as one of the injurious factors in H. pylori-colonized gastric mucosa, the present study is designed to investigate the level of stress-induced gastric mucosal oxidative injury with or without intragastric NH3 overloading. To apply emotional stress, the communication box paradigm was used in the mouse model. Mice (C57BL/6, male) were pretreated with distilled water (responder-H2O) or 0.01% NH3 (responder-NH3) through a gastric tube once a day for a week. Emotional stress was then applied to the responder mice for 3 h per day for 3 d by watching and hearing the behavior of the sender mice subjected to electric shocks to the feet (2 mA, 10 s, 50 s interval). After the communication box protocol, the tissue MPO activity, the contents of TBA-reactive substances (TBARS), and the level of gastric mucosal HSP70 were examined. Responder-NH3 mice developed more severe gastric lesions than the responder-H2O subjects. MPO activity and TBARS contents were enhanced significantly in the responder-NH3 group compared with the responder-H2O subjects. Although the contents of HSP70 in the gastric mucosa increased in the responder-H2O group compared with the control-H2O animals, they were significantly attenuated in the responder-NH3 mice. Excess intragastric NH3 was able to enhance the formation of emotional stress-induced gastric mucosal lesions. This injury may be associated with the enhanced production of oxygen free radicals from accumulated neutrophils under the NH3-mediated cancellation of gastric mucosal cytoprotective HSP70.

Original languageEnglish
Pages (from-to)1073-1081
Number of pages9
JournalFree Radical Biology and Medicine
Volume33
Issue number8
DOIs
Publication statusPublished - 2002 Oct 15

Fingerprint

HSP70 Heat-Shock Proteins
Ammonia
Stomach
Communication
Wounds and Injuries
Audition
Free Radicals
Psychological Stress
Animals
Tissue
Oxygen
Gastric Mucosa
Water
Helicobacter pylori
Mucous Membrane
Inbred C57BL Mouse
Hearing
Foot
Shock
Reactive Oxygen Species

Keywords

  • Free radicals
  • Heat shock protein 70
  • Helicobacter pylori
  • Lipid peroxide
  • Myeloperoxidase

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry

Cite this

Ammonia aggravates stress-induced gastric mucosal oxidative injury through the cancellation of cytoprotective heat shock protein 70. / Nagahashi, Shoichi; Suzuki, Hidekazu; Miyazawa, Masaharu; Nagata, Hiroshi; Suzuki, Masayuki; Miura, Soichiro; Ishii, Hiromasa.

In: Free Radical Biology and Medicine, Vol. 33, No. 8, 15.10.2002, p. 1073-1081.

Research output: Contribution to journalArticle

Nagahashi, Shoichi ; Suzuki, Hidekazu ; Miyazawa, Masaharu ; Nagata, Hiroshi ; Suzuki, Masayuki ; Miura, Soichiro ; Ishii, Hiromasa. / Ammonia aggravates stress-induced gastric mucosal oxidative injury through the cancellation of cytoprotective heat shock protein 70. In: Free Radical Biology and Medicine. 2002 ; Vol. 33, No. 8. pp. 1073-1081.
@article{78443b5021e543aab99da06068e7af49,
title = "Ammonia aggravates stress-induced gastric mucosal oxidative injury through the cancellation of cytoprotective heat shock protein 70",
abstract = "The relationship between Helicobacter pylori colonization and the formation of stress-induced gastric mucosal injury remains unknown. Since ammonia (NH3) is known as one of the injurious factors in H. pylori-colonized gastric mucosa, the present study is designed to investigate the level of stress-induced gastric mucosal oxidative injury with or without intragastric NH3 overloading. To apply emotional stress, the communication box paradigm was used in the mouse model. Mice (C57BL/6, male) were pretreated with distilled water (responder-H2O) or 0.01{\%} NH3 (responder-NH3) through a gastric tube once a day for a week. Emotional stress was then applied to the responder mice for 3 h per day for 3 d by watching and hearing the behavior of the sender mice subjected to electric shocks to the feet (2 mA, 10 s, 50 s interval). After the communication box protocol, the tissue MPO activity, the contents of TBA-reactive substances (TBARS), and the level of gastric mucosal HSP70 were examined. Responder-NH3 mice developed more severe gastric lesions than the responder-H2O subjects. MPO activity and TBARS contents were enhanced significantly in the responder-NH3 group compared with the responder-H2O subjects. Although the contents of HSP70 in the gastric mucosa increased in the responder-H2O group compared with the control-H2O animals, they were significantly attenuated in the responder-NH3 mice. Excess intragastric NH3 was able to enhance the formation of emotional stress-induced gastric mucosal lesions. This injury may be associated with the enhanced production of oxygen free radicals from accumulated neutrophils under the NH3-mediated cancellation of gastric mucosal cytoprotective HSP70.",
keywords = "Free radicals, Heat shock protein 70, Helicobacter pylori, Lipid peroxide, Myeloperoxidase",
author = "Shoichi Nagahashi and Hidekazu Suzuki and Masaharu Miyazawa and Hiroshi Nagata and Masayuki Suzuki and Soichiro Miura and Hiromasa Ishii",
year = "2002",
month = "10",
day = "15",
doi = "10.1016/S0891-5849(02)00998-X",
language = "English",
volume = "33",
pages = "1073--1081",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "Elsevier Inc.",
number = "8",

}

TY - JOUR

T1 - Ammonia aggravates stress-induced gastric mucosal oxidative injury through the cancellation of cytoprotective heat shock protein 70

AU - Nagahashi, Shoichi

AU - Suzuki, Hidekazu

AU - Miyazawa, Masaharu

AU - Nagata, Hiroshi

AU - Suzuki, Masayuki

AU - Miura, Soichiro

AU - Ishii, Hiromasa

PY - 2002/10/15

Y1 - 2002/10/15

N2 - The relationship between Helicobacter pylori colonization and the formation of stress-induced gastric mucosal injury remains unknown. Since ammonia (NH3) is known as one of the injurious factors in H. pylori-colonized gastric mucosa, the present study is designed to investigate the level of stress-induced gastric mucosal oxidative injury with or without intragastric NH3 overloading. To apply emotional stress, the communication box paradigm was used in the mouse model. Mice (C57BL/6, male) were pretreated with distilled water (responder-H2O) or 0.01% NH3 (responder-NH3) through a gastric tube once a day for a week. Emotional stress was then applied to the responder mice for 3 h per day for 3 d by watching and hearing the behavior of the sender mice subjected to electric shocks to the feet (2 mA, 10 s, 50 s interval). After the communication box protocol, the tissue MPO activity, the contents of TBA-reactive substances (TBARS), and the level of gastric mucosal HSP70 were examined. Responder-NH3 mice developed more severe gastric lesions than the responder-H2O subjects. MPO activity and TBARS contents were enhanced significantly in the responder-NH3 group compared with the responder-H2O subjects. Although the contents of HSP70 in the gastric mucosa increased in the responder-H2O group compared with the control-H2O animals, they were significantly attenuated in the responder-NH3 mice. Excess intragastric NH3 was able to enhance the formation of emotional stress-induced gastric mucosal lesions. This injury may be associated with the enhanced production of oxygen free radicals from accumulated neutrophils under the NH3-mediated cancellation of gastric mucosal cytoprotective HSP70.

AB - The relationship between Helicobacter pylori colonization and the formation of stress-induced gastric mucosal injury remains unknown. Since ammonia (NH3) is known as one of the injurious factors in H. pylori-colonized gastric mucosa, the present study is designed to investigate the level of stress-induced gastric mucosal oxidative injury with or without intragastric NH3 overloading. To apply emotional stress, the communication box paradigm was used in the mouse model. Mice (C57BL/6, male) were pretreated with distilled water (responder-H2O) or 0.01% NH3 (responder-NH3) through a gastric tube once a day for a week. Emotional stress was then applied to the responder mice for 3 h per day for 3 d by watching and hearing the behavior of the sender mice subjected to electric shocks to the feet (2 mA, 10 s, 50 s interval). After the communication box protocol, the tissue MPO activity, the contents of TBA-reactive substances (TBARS), and the level of gastric mucosal HSP70 were examined. Responder-NH3 mice developed more severe gastric lesions than the responder-H2O subjects. MPO activity and TBARS contents were enhanced significantly in the responder-NH3 group compared with the responder-H2O subjects. Although the contents of HSP70 in the gastric mucosa increased in the responder-H2O group compared with the control-H2O animals, they were significantly attenuated in the responder-NH3 mice. Excess intragastric NH3 was able to enhance the formation of emotional stress-induced gastric mucosal lesions. This injury may be associated with the enhanced production of oxygen free radicals from accumulated neutrophils under the NH3-mediated cancellation of gastric mucosal cytoprotective HSP70.

KW - Free radicals

KW - Heat shock protein 70

KW - Helicobacter pylori

KW - Lipid peroxide

KW - Myeloperoxidase

UR - http://www.scopus.com/inward/record.url?scp=0037108205&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037108205&partnerID=8YFLogxK

U2 - 10.1016/S0891-5849(02)00998-X

DO - 10.1016/S0891-5849(02)00998-X

M3 - Article

VL - 33

SP - 1073

EP - 1081

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

IS - 8

ER -