Differential expression of neuronal and inducible nitric oxide synthase in rat brain after subchronic administration of 3-monochloro-1,2-propanediol

2008 ◽  
Vol 46 (3) ◽  
pp. 955-960 ◽  
Author(s):  
Kisok Kim
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Differential Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Dynamics of Nitrotyrosine Formation and Decay in Rat Brain during Focal Ischemia-Reperfusion

1999 ◽  
Vol 19 (6) ◽  
pp. 667-672 ◽  
Author(s):  
Shunya Takizawa ◽  
Naoto Fukuyama ◽  
Hisayuki Hirabayashi ◽  
Hiroe Nakazawa ◽  
Yukito Shinohara
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Inducible Nitric Oxide Synthase ◽  
Time Window ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Focal Ischemia ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The purpose of this study was to establish the dynamics of nitrotyrosine (NO2-Tyr) formation and decay during the rise of NO2-Tyr in rat brain subjected to 2-hour focal ischemia-reperfusion, and to evaluate the role of inducible nitric oxide synthase in the rise. The authors first determined the half life of NO2-Tyr in rat brain at 24 hours after the start of reperfusion by blocking NO2-Tyr formation with NG-monomethyl-l-arginine and after the decay of NO2-Tyr by means of a hydrolysis/HPLC procedure. The values obtained were approximately 2 hours in both peri-infarct and core-of-infarct regions. Using the same hydrolysis/HPLC procedure, the ratio of nitrotyrosine to tyrosine from the 2-hour occlusion to as much as 72 hours after the start of reperfusion was measured in the presence and absence of aminoguanidine (100 mg/kg intraperitoneally twice a day). In the absence of aminoguanidine, the ratio of NO2-Tyr in the peri-infarct and core-of-infarct regions reached 0.95% ± 0.34% and 0.52% ± 0.34%, respectively, at 1 hour after the start of reperfusion, The elevated levels persisted until 48 hours, then declined, The peri-infarct region showed the highest percent NO2-Tyr level, followed by the core of infarct, then the caudoputamen, Aminoguanidine significantly reduced NO2-Tyr formation (up to 90% inhibition) during 24 to 48 hours, The authors conclude that inducible nitric oxide synthase is predominantly responsible for NO2-Tyr formation, at least in the late phase of reperfusion, These results have important implications for the therapeutic time window and choice of nitric oxide synthase inhibitors in patients with cerebral infarction.

scholarly journals Chronic Stress Induces the Expression of Inducible Nitric Oxide Synthase in Rat Brain Cortex

2001 ◽  
Vol 74 (2) ◽  
pp. 785-791 ◽  
Author(s):  
Raquel Olivenza ◽  
María A. Moro ◽  
Ignacio Lizasoain ◽  
Pedro Lorenzo ◽  
Ana P. Fernández ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Chronic Stress ◽  
Inducible Nitric Oxide Synthase ◽  
Brain Cortex ◽  
Rat Brain Cortex ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide
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