Korean J Physiol Pharmacol.  2001 Jun;5(3):205-212.

Increase of peroxynitrite production in the rat brain following transient forebrain ischemia

• Kim HJ
• Kim SY

Abstract

It has been proposed that nitric oxide is involved in the pathogenesis of cerebral ischemia-reperfusion. Because superoxide production is also enhanced during reperfusion, the cytotoxic oxidant peroxynitrite could be formed, but it is not known if this occurs following global forebrain ischemia-reperfusion. We examined whether peroxynitrite generation is increased in the vulnerable regions after forebrain ischemia-reperfusion. Transient forebrain ischemia was produced in the conscious rat by four-vessel occlusion. Rats were subjected to 10 or 15 min of forebrain ischemia. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion. Furthermore, in rats subjected to ischemia for 15 min, this change was also observed in the lateral striatal region and the lateral septal nucleus 2apprx3 days after reperfusion. The cresyl violet staining of adjacent sections showed that neuronal cell death was induced in parallel with the nitrotyrosine immunoreactivity in the hippocampal CA1 area and the lateral striatal region. Our findings suggest that oxygen free radical accumulation and consequent peroxynitrite production play a role in neuronal death caused by cerebral ischemia-reperfusion.

MeSH Terms

Animals
Brain*
Cell Death
Ischemia*
Neurons
Nitric Oxide
Oxygen
Peroxynitrous Acid*
Prosencephalon*
Rats*
Reperfusion
Septal Nuclei
Superoxides
Viola
Nitric Oxide
Oxygen
Peroxynitrous Acid
Superoxides