In vivo EPR imaging by using an acyl-protected hydroxylamine to analyze intracerebral oxidative stress in rats after epileptic seizures

EPR imaging by using an acyl-protected hydroxylamine, 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP), in the head of a living rat after kainic acid (KA)-induced epileptic seizures was performed. ACP is a stable non-radical compound, but is easily deprotected with intracellular esterase t...

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Bibliographic Details
Published in:Magnetic resonance imaging 2000-09, Vol.18 (7), p.875-879
Main Authors: Yokoyama, Hidekastu, Itoh, Osamu, Aoyama, Masaaki, Obara, Heitaro, Ohya, Hiroaki, Kamada, Hitoshi
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain
Cerebral Cortex - metabolism
Cerebral Cortex - pathology
Corpus Striatum - metabolism
Corpus Striatum - pathology
Disease Models, Animal
Electron Spin Resonance Spectroscopy
EPR imaging
Hippocampus - metabolism
Hippocampus - pathology
Image Enhancement - methods
In vivo
Investigative techniques, diagnostic techniques (general aspects)
Kainic Acid
Male
Medical sciences
Nervous system
Oxidative Stress
Phantoms, Imaging
Pyrrolidines - pharmacokinetics
Radionuclide investigations
Rats
Rats, Wistar
Reference Values
Seizures - chemically induced
Seizures - metabolism
Sensitivity and Specificity
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Summary:EPR imaging by using an acyl-protected hydroxylamine, 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP), in the head of a living rat after kainic acid (KA)-induced epileptic seizures was performed. ACP is a stable non-radical compound, but is easily deprotected with intracellular esterase to yield a hydroxylamine, which is oxidized by intracellular oxidative stress to yield an EPR-detectable nitroxide radical. From in vivo image data, the average values of EPR signal intensity from the hippocampus, striatum, and cerebral cortex were computed. There was no significant difference in cortical signal intensity between the control and KA-treated rats. The signal intensities from the hippocampus and striatum for the KA-treated rats were significantly higher than those for the control. The in vitro study showed that almost the same quantity of ACP moved into all regions of the brain of the control and KA-treated rats. These findings indicate that following a KA-induced seizure, the oxidative stress in the hippocampus and striatum is enhanced, but not so in the cerebral cortex.
ISSN:0730-725X
1873-5894
DOI:10.1016/S0730-725X(00)00183-1