In order to analyze free radical reactions in living stomach, we developed a noninvasive measurement by an in vivo electron spin resonance (ESR) and spin probe technique and applied it to mucosal injury. NH4OH-induced gastric lesions were prepared in rats. A nitroxyl probe was administered intragastrically or intravenously, and then in vivo ESR spectra of the gastric region were obtained by 300 MHz ESR spectroscopy. The signal of the intragastrically administered spin probe decreased gradually and the decay significantly enhanced 30 min after NH4OH administration. The enhanced signal decay was attributed to the OH radical generation, since it was completely suppressed by mannitol, catalase, and desferrioxamine. Two commercially available antigastric lesion drugs, rebamipide and taurine, were tested with a NH4OH-induced gastric lesion model. Both intraperitoneal administration of rebamipide and intravenous administration of taurine suppressed gastric lesion formation induced by NH4OH in a dose-dependent manner. Intraperitoneal preadministration of rebamipide also suppressed the enhanced signal decay, but neither pre- nor coadministration of taurine showed any effect on the enhanced signal decay. The results strongly indicate that the inhibitory mechanism on gastric lesion formation in NH4OH-treated rats is quite different for the two antigastric lesion drugs rebamipide and taurine.
All Science Journal Classification (ASJC) codes
- Atomic and Molecular Physics, and Optics