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-tetramethypyrrolidine (ACP), in the head of a living rat after kai nic 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 cort ical signal intensity between the control and KA-treated rats. The signal i ntensities From the hippocampus and striatum for the KA-treated rats were s ignificantly higher than those for the control. The in vitro study showed t hat 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 K A-induced seizure, the oxidative stress in the hippocampus and striatum is enhanced, but not so in the cerebral cortex. (C) 2000 Elsevier Science Inc. All rights reserved.