7-Nitroindazole attenuates nitrotyrosine formation in the early phase of cerebral ischemia-reperfusion in mice.

Abstract

The purpose of this study was to evaluate the role of neuronal nitric oxide synthase (nNOS) in nitrotyrosine (NO2-Tyr) formation in the early phase of ischemia-reperfusion in mouse brain. Using a hydrolysis/high pressure liquid chromatography (HPLC) procedure (0.6 microM detection limit), we measured %NO2-Tyr (ratio of NO2-Tyr to total tyrosine) in 23 male C57Black/6J mice subjected to 2-h middle cerebral artery occlusion followed by 0.5-h reperfusion, in the presence (25 or 50 mg/kg) and absence of 7-nitroindazole (7-NI), a relatively specific nNOS inhibitor. At 25 mg/kg, 7-NI reduced NO2-Tyr formation to about a half of that in the vehicle-treated group (0.10 +/- 0.07 vs. 0.18 +/- 0.05%), while 50 mg/kg suppressed NO2-Tyr formation to below the limit of detection, indicating that nNOS is responsible for most of the NO2-Tyr formation in the early phase after reperfusion.

• Authors: H Hirabayashi, S Takizawa, N Fukuyama, H Nakazawa, Y Shinohara
• Journal: Neuroscience letters (Neurosci Lett) Vol. 268 Issue 2 Pg. 111-3 (Jun 18 1999) ISSN: 0304-3940 [Print] Ireland
• PMID: 10400091 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Indazoles
• Neuroprotective Agents
• 3-nitrotyrosine
• Tyrosine
• 7-nitroindazole

Topics

• Animals
• Brain Ischemia (metabolism)
• Chromatography, High Pressure Liquid
• Indazoles (pharmacology)
• Male
• Mice
• Mice, Inbred C57BL
• Neuroprotective Agents (pharmacology)
• Reperfusion Injury (metabolism)
• Tyrosine (analogs & derivatives, metabolism)