Non-invasive analysis of reactive oxygen species generated in rats with water immersion restraint-induced gastric lesions using in vivo electron spin resonance spectroscopy

Keiji Yasukawa, Keiko Kasazaki, Fuminori Hyodo, Hideo Utsumi

    Research output: Contribution to journalReview article

    51 Citations (Scopus)

    Abstract

    Reactive oxygen species (ROS) are reportedly associated with gastric ulcer. We previously reported the use of an in vivo 300-MHz electron spin resonance (ESR) spectroscopy/nitroxyl probe technique to detect OH generation in the stomachs of rats with gastric ulcers induced by NH4OH. However, this is an acute ulcer model, and the relationship between in vivo ROS generation and lesion formation remains to be clarified. To address this question, the same technique was applied to a sub-acute water immersion restraint (WIR model. A nitroxyl probe that was less membrane-permeable was orally administered to WIR-treated rats, and the spectra in the gastric region were obtained by in vivo ESR spectroscopy. The signal intensity of the orally administered probe was clearly changed in the WIR group, but no change occurred in the control group. Both enhanced signal decay and neutrophil infiltration into mucosa were observed 2 h after WIR with little formation of any mucosal lesions. The enhanced signal decay was caused by OH generation, based on the finding that the decay was suppressed by mannitol, desferrioxamine and catalase. Intravenous treatment with either anti-neutrophil antibody or allopurinol also suppressed the enhanced signal decay, and allopurinol depressed neutrophil infiltration into the mucosa. In rats treated with WIR for 6 h, lesion formation was suppressed by 50% with all antioxidants used in this experiment except anti-neutrophil antibody. These findings suggest that OH, which is generated in the stomach via the hypoxanthine/xanthine oxidase system upon neutrophil infiltrated into the mucosa, induces mucosal lesion formation, but that it accounts for only half the cause of lesion formation.

    Original languageEnglish
    Pages (from-to)147-155
    Number of pages9
    JournalFree Radical Research
    Volume38
    Issue number2
    DOIs
    Publication statusPublished - Feb 1 2004

    Fingerprint

    Electron spin resonance spectroscopy
    Electron Spin Resonance Spectroscopy
    Immersion
    Rats
    Reactive Oxygen Species
    Stomach
    Mucous Membrane
    Allopurinol
    Neutrophils
    Neutrophil Infiltration
    Stomach Ulcer
    Infiltration
    Water
    Anti-Idiotypic Antibodies
    Deferoxamine
    Antibodies
    Xanthine Oxidase
    Mannitol
    Catalase
    Ulcer

    All Science Journal Classification (ASJC) codes

    • Biochemistry

    Cite this

    Non-invasive analysis of reactive oxygen species generated in rats with water immersion restraint-induced gastric lesions using in vivo electron spin resonance spectroscopy. / Yasukawa, Keiji; Kasazaki, Keiko; Hyodo, Fuminori; Utsumi, Hideo.

    In: Free Radical Research, Vol. 38, No. 2, 01.02.2004, p. 147-155.

    Research output: Contribution to journalReview article

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    abstract = "Reactive oxygen species (ROS) are reportedly associated with gastric ulcer. We previously reported the use of an in vivo 300-MHz electron spin resonance (ESR) spectroscopy/nitroxyl probe technique to detect •OH generation in the stomachs of rats with gastric ulcers induced by NH4OH. However, this is an acute ulcer model, and the relationship between in vivo ROS generation and lesion formation remains to be clarified. To address this question, the same technique was applied to a sub-acute water immersion restraint (WIR model. A nitroxyl probe that was less membrane-permeable was orally administered to WIR-treated rats, and the spectra in the gastric region were obtained by in vivo ESR spectroscopy. The signal intensity of the orally administered probe was clearly changed in the WIR group, but no change occurred in the control group. Both enhanced signal decay and neutrophil infiltration into mucosa were observed 2 h after WIR with little formation of any mucosal lesions. The enhanced signal decay was caused by •OH generation, based on the finding that the decay was suppressed by mannitol, desferrioxamine and catalase. Intravenous treatment with either anti-neutrophil antibody or allopurinol also suppressed the enhanced signal decay, and allopurinol depressed neutrophil infiltration into the mucosa. In rats treated with WIR for 6 h, lesion formation was suppressed by 50{\%} with all antioxidants used in this experiment except anti-neutrophil antibody. These findings suggest that •OH, which is generated in the stomach via the hypoxanthine/xanthine oxidase system upon neutrophil infiltrated into the mucosa, induces mucosal lesion formation, but that it accounts for only half the cause of lesion formation.",
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