Role of nitric oxide as an antioxidant in the defense of gastric cells

H. Kim, E. Lee, K. H. Kim

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Gatric mucosa is exposed to toxic, reactive oxygen species generated within the lumen. Nitric oxide protected acetaminophen-induced hepatotoxicity by maintaining glutathione homeostasis. The present study examined the role of nitric oxide in mediating hydrogen peroxide-induced damage to gastric cells. Hydrogen peroxide was generated by glucose oxidase acting on β-D-glucose. L-arginine, N(G)-nitro-L-arginine methyl ester, or N(G)-nitro-L-arginine were treated to the cells with glucose/glucose oxidase. Lipid peroxidation and nitrite release and cellular content of glutathione were determined. As a result, dose-dependent increase in lipid peroxide production as well as dose-dependent decrease in nitrite release and cellular glutathione content were observed in glucose/glucose oxidase-treated cells. Pretreatment of L-arginine, a substrate for nitric oxide synthase, prevented the increase of lipid peroxide production and the reduction of nitrite release as well as glutathione content. Inhibitors of nitric oxide synthase such as N(G)-nitro-L-arginine methyl ester and N(G)-nitro-L-arginine did not protect hydrogen peroxide-induced cell damage. In conclusion, nitric oxide protects gastric cells from hydrogen peroxide possibly by inhibiting lipid peroxidation and by preserving cellular glutathione stores.

Original languageEnglish
Pages (from-to)389-397
Number of pages9
JournalKorean Journal of Pharmacology
Volume32
Issue number3
Publication statusPublished - 1996 Dec 1

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Glutathione
Stomach
Nitric Oxide
Antioxidants
Glucose Oxidase
Hydrogen Peroxide
Arginine
Nitrites
Lipid Peroxides
NG-Nitroarginine Methyl Ester
Glucose
Nitric Oxide Synthase
Lipid Peroxidation
Poisons
Acetaminophen
Reactive Oxygen Species
Mucous Membrane
Homeostasis

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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title = "Role of nitric oxide as an antioxidant in the defense of gastric cells",
abstract = "Gatric mucosa is exposed to toxic, reactive oxygen species generated within the lumen. Nitric oxide protected acetaminophen-induced hepatotoxicity by maintaining glutathione homeostasis. The present study examined the role of nitric oxide in mediating hydrogen peroxide-induced damage to gastric cells. Hydrogen peroxide was generated by glucose oxidase acting on β-D-glucose. L-arginine, N(G)-nitro-L-arginine methyl ester, or N(G)-nitro-L-arginine were treated to the cells with glucose/glucose oxidase. Lipid peroxidation and nitrite release and cellular content of glutathione were determined. As a result, dose-dependent increase in lipid peroxide production as well as dose-dependent decrease in nitrite release and cellular glutathione content were observed in glucose/glucose oxidase-treated cells. Pretreatment of L-arginine, a substrate for nitric oxide synthase, prevented the increase of lipid peroxide production and the reduction of nitrite release as well as glutathione content. Inhibitors of nitric oxide synthase such as N(G)-nitro-L-arginine methyl ester and N(G)-nitro-L-arginine did not protect hydrogen peroxide-induced cell damage. In conclusion, nitric oxide protects gastric cells from hydrogen peroxide possibly by inhibiting lipid peroxidation and by preserving cellular glutathione stores.",
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Role of nitric oxide as an antioxidant in the defense of gastric cells. / Kim, H.; Lee, E.; Kim, K. H.

In: Korean Journal of Pharmacology, Vol. 32, No. 3, 01.12.1996, p. 389-397.

Research output: Contribution to journalArticle

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AB - Gatric mucosa is exposed to toxic, reactive oxygen species generated within the lumen. Nitric oxide protected acetaminophen-induced hepatotoxicity by maintaining glutathione homeostasis. The present study examined the role of nitric oxide in mediating hydrogen peroxide-induced damage to gastric cells. Hydrogen peroxide was generated by glucose oxidase acting on β-D-glucose. L-arginine, N(G)-nitro-L-arginine methyl ester, or N(G)-nitro-L-arginine were treated to the cells with glucose/glucose oxidase. Lipid peroxidation and nitrite release and cellular content of glutathione were determined. As a result, dose-dependent increase in lipid peroxide production as well as dose-dependent decrease in nitrite release and cellular glutathione content were observed in glucose/glucose oxidase-treated cells. Pretreatment of L-arginine, a substrate for nitric oxide synthase, prevented the increase of lipid peroxide production and the reduction of nitrite release as well as glutathione content. Inhibitors of nitric oxide synthase such as N(G)-nitro-L-arginine methyl ester and N(G)-nitro-L-arginine did not protect hydrogen peroxide-induced cell damage. In conclusion, nitric oxide protects gastric cells from hydrogen peroxide possibly by inhibiting lipid peroxidation and by preserving cellular glutathione stores.

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