In vivo ESR measurements were carried out to estimate free radical reactions in living mice using nitroxyl radicals as probes. The ESR signal of nitroxyl radical which was intravenously or intramuscularly injected to living female ddY mice decreased gradually by reducing to the corresponding hydroxylamine. The reduction rate was enhanced by oxidative stress, and pre-treatment of antioxidants suppressed the enhancement of signal decay. Oral administration of carbon tetrachloride enhanced signal decay in upper abdomen but not m thorax. These results indicated that free radicals, which can reduce nitroxyl radical, were produced in the upper abdomen by oral administration of carbon tetrachloride.
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